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Rnnlc F A 5 _ 

Copyright N°_ 


COPYRIGHT DEPOSIT. 



















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Tuberculosis of Knee. Resection, with removal of about one centimeter from the end of femur and tibia. 
(T). Joint surface of tibia. (C). Cut surface of resected piece of tibia. 

( B ). Joint surface of femur. ( D ). Cut surface of resected piece of femur. Note sequestrum. 




INFLAMMATION IN 
BONES AND JOINTS 


BY 

LEONARD W. ELY, M.D. 

ASSOCIATE PROFESSOR OF SURGERY, STANFORD UNIVERSITY 




144 ILLUSTRATIONS 



) 

i 

) 


PHILADELPHIA AND LONDON 
J. B. LIPPINCOTT COMPANY 



COPYRIGHT, 1923, BY J. B. LIPPINCOTT COMPANY 


PRINTED BY J. B. LIPPINCOTT COMPANY 
AT THE WASHINGTON SQUARE PRESS, 
PHILADELPHIA, U. S. A. 


©C1A705131 

APR 27 ’23 

'KO 1 








TO MY WIFE 




PREFACE 

To write a book on inflammation in bones and joints 
requires considerable temerity, and, perhaps, if I disown 
any undue self-confidence, I shall disarm criticism in ad¬ 
vance. Unlike many subjects in medicine, great difference 
of opinion exists as to the physiology and pathology of 
these two organs. We have abundant clinical material 
on which to draw, but conclusions based on clinical opin¬ 
ion are notoriously conflicting. Like a religious argument, 
and perhaps for the same reason, an argument between 
the exponents of diverse clinical views is usually character¬ 
ized by positive statement and by some acrimony. 

We have at our disposal also the results of considerable 
investigative work, but much of this is not as well known as 
it should be, and the conclusions of the investigators do 
not always agree. Too often the laboratory worker does 
not take the trouble to check up his results by clinical 
evidence, and too often the clinical expert is unwilling 
to devote the time in the laboratory which is necessary 

«/ V 

if he would understand the fundamental processes in the 
tissues with which he deals. Without this knowledge he 
is simply guessing as to what lies beneath the surface. 

When all is said, the gap in our knowledge is due to 
our ignorance of bone pathology, and we shall probably 
not fill it up until bones and joints are sectioned at necropsy 
with the same care as are other organs. We may not 
always agree with an observer’s conclusions, but we all 
know, when we are searching through a mass of contradic¬ 
tory opinions, with what satisfaction we greet the publica¬ 
tion of concrete, definite facts discovered in the examination 
of pathological material. We can draw our own conclu¬ 
sions from these facts. 


G 


PREFACE 


Whatever this book lacks must be charged to the 
limitations of its author. It is based upon personal obser¬ 
vation and research, and is not to be regarded as a 
compilation, though on numerous occasions I have taken 
pains to set forth the opinions of others where they differ 
from mine. The chief merit, I think, is its exposition 
of the results of original research, and of work in the 
pathological laboratory, and the correlation of this work 
with clinical findings. The facts unearthed in this way 
should be of value to others, even when the conclusions 
drawn from them are not accepted. 

My colleagues in the Stanford Medical School, by 
their cooperation and encouragement have aided me in 
many ways, particularly Dr. Frank Blaisdell, Associate 
Professor of Surgery, in my animal work and in the illus¬ 
trations. I am under great obligation to the librarians 
of the Lane Library, for their unremitting work upon the 
bibliographies, which should be of the greatest help to the 
student. The devoted work of my technician. Miss 
Wallach is beyond all praise. 

The facilities which Stanford University puts at the dis¬ 
posal of its faculty are unique. As tools it furnishes a great 
library, laboratories, clinics and hospitals, all grouped 
closely, and grants the leisure to use them. To its president 
and trustees I make my respectful acknowledgments. 

I take pleasure in acknowledging my indebtedness to 
Messrs. William Wood & Company of New York, to the 
Surgery Publishing Company of New York, and to the 
editors of The Annals of Surgery, the Archives of Surgery 
and the Journal of the American Medical Association for 
permission to reproduce material which has appeared in 
their publications. 

San Francisco, California, 1923. 


The Author. 


CONTENTS 

SECTION I. 

GENERAL CONSIDERATIONS. 

CHAPTER PAGE 

I. General Considerations. 15 

SECTION II. 

ACUTE OSTEOMYELITIS AND ARTHRITIS. 

I. Acute Suppurative Hematogenous Osteomyelitis. 79 

II. Acute Suppurative Hematogenous Arthritis. 94 

III. Suppurative Osteomyelitis Following Compound Fracture. 99 

,, IV. Typhoid Osteomyelitis and Arthritis. 100 

V. Gonococcic Osteomyelitis and Arthritis. 103 

VI. Acute Inflammatory Rheumatism. 108 

VII. Hydrarthrosis Intermittens. 110 

VIII. Traumatic Arthritis. :... 112 

IX. Suppurative Arthritis from Wounds. 120 

X. Hemophiliac Joints. 123 

SECTION III. 

CHRONIC OSTEOMYELITIS. 

I. Phosphorus Necrosis. 133 

II. Syphilis. 135 

III. Chronic Osteomyelitis of Unknown Origin. 147 

Osteomyelitis Fibrosa. 147 

Paget's Deforming Osteomyelitis, Ostitis Deformans 148 

Leontiasis Ossea 155 

Osteomyelitis Fibrosa, Ostitis Fibrosa 155 

Pulmonary Hypertrophic Osteoarthropathy 156 

IV. Rickets, Rhachitis. 158 

SECTION IV. 

CHRONIC ARTHRITIS. 

The Two Great Types. Joint Tuberculosis in General. 173 

The First Great Type of Chronic Arthritis, Tuberculous 

Arthritis. 177 

7 




















8 


CONTENTS 
SECTION V. 

TUBERCULOSIS OF SPECIAL JOINTS 


CHAPTER PAGE 

I. Tuberculosis of the Spine, Pott's disease. 237 

II. Tuberculosis of the Hip. 272 

III. Tuberculosis of the Knee. 295 

IV. Tuberculosis of the Ankle and Tarsus. 308 

V. Tuberculosis of the Shoulder. 317 

VI. Tuberculosis of the Elbow. 322 

VII. Tuberculosis of the Wrist. 326 

VIII. Tuberculosis of the Sacro-Iliac Joint. 331 

IX. Tuberculosis of the Fingers and Toes. 337 

SECTION VI. 

OTHER FORMS OF ARTHRITIS OF THE FIRST 

GREAT TYPE OR GROUP. 

I. Coccidioidal Granuloma. 345 

II. Chronic Diplostreptococcic Arthritis. 349 

III. Chronic Progressive Multiple Arthritis. 357 

IV. Still's Disease. 360 

SECTION VII. 

THE SECOND GREAT TYPE OF 
CHRONIC ARTHRITIS. 

I. The Second Great Type of Chronic Arthritis. 365 

SECTION VIII. 

ARTHRITIS CAUSED BY DEVELOP¬ 
MENTAL ABNORMALITIES. 

I. Legg's Disease,. 401 

II. Loose Bodies in the Joint, Joint Mouse, Osteochondritis Dissecans 409 

III. Koehler’s Disease. 418 

IV. OsGOOD-ScHLATTER DISEASE. 420 

Index of Authors. 420 

Index. 431 





















FIG. 


ILLUSTRATIONS 


PAGE 

L Slice of the distal portion of the normal human femur. 16 

2. Low-power photomicrograph showing blood vessel entering the bone 

cortex . 17 

3. Marrow pocket on the outside of the cortex. 19 

4. Low-power photomicrograph of diffuse tuberculosis in the bone 

marrow . 21 

5. Low-power photomicrograph of normal human bone, showing peri¬ 

osteum and fairly dense bone. 23 

6. Photograph of stained slide from a sagittal section of the knee of 

a normal dog. 25 

7. Section of dog's patella, camera lucida drawing. 27 

8. Low-power photomicrograph, showing typical appearance of the 

synovial membrane in an acute inflammation. 29 

9. Low-power photomicrograph from a case of marrow tuberculosis.... 33 

10. High-power photomicrograph of a portion of the preceding slide.... 34 

11. Low-power photomicrograph from a case of acute suppurative arthritis 35 

12. Low-power photomicrograph from the knee joint of a foetus at term 37 

13. Low-power photomicrograph of early stage of intracartilaginous 

bone formation. 38 

14. Low-power photomicrograph from a stained slide taken from a section 

of the outside of the cortex of the tibia of a dog. 43 

15. Photograph of a stained slide from a sagittal section of the knee 

of a dog. 44 

16. Photograph of stained slide from sagittal section of knee of dog, 

resected 374 days previously. 45 

17. Photograph of stained slide of sagittal section of knee of dog, re¬ 

sected twenty-seven days previously. 46 

18. Photograph of a stained slide from a sagittal section of the knee of 

a dog, resected 150 days previously. 47 

19. Photograph of a stained slide from a sagittal section of the knee of 

a dog, resected 790 days previously. 48 

20. Photograph of stained slide from sagittal section of knee of dog, 

resected 922 days previously. 49 

21. Stained slide of section of piece of condyle of femur buried fresh 

in the thigh muscles of the animal from whom it had just been 
removed; 922 days after burying. 50 

22. Stained slide of section of piece of head of tibia. 51 

23. Photograph of stained slide of section of a piece of the condyle. 51 

24. Photograph of a stained slide of a cross-section of a fragment of 

the femoral condyle. 51 

25. Cross-section of piece of condyle of femur. 52 

26. Section of condyle femur of dog, removed at knee joint resection.... 54 

27. Low-power photomicrograph of the bone in inked square in the pre¬ 

ceding illustration. 55 


9 

























10 


ILLUSTRATIONS 


28. Showing how the large fragment is slid across into the gap left by 

the removal of the small one. 

29. Low-power photomicrograph of stained slide from a tibial graft used 

in an Albee spine operation. 58 

30. Low-power photomicrograph of a pseudarthrosis between a bone 

graft and the bone into which it is doweled. 59 

31. Bony ankylosis of wrist following an old closed infectious arthritis.. 62 

32. Old fibrocartilaginous ankylosis of the elbow-joint. 63 

33. Tuberculous knee, ten years after resection. 65 

34. Ankylosis caused by new bone in the joint capsule. 66 

35. Acute suppurative hoematogenous osteomyelitis of the femur. 86 

36. Acute suppurative haematogenous osteomyelitis of the clavicle. 87 

37. Photomicrograph of bone and cartilage from a section of acute 

suppurative arthritis. 94 

38 Suppurative inflammation in the bone marrow in the region of the joint. 95 

39. The so-called gonorrheal periostitis of the tubercle of the calcaneus.. 106 

40. Hsemarthrosis of the knee in a “bleeder”. 124 

41. Skiagram of a case of old fibrous ankylosis in a “bleeder”. 125 

42. Dactylitis, probably syphilitic, but treated for a long time as tuber¬ 

culosis . 140 

43. Bone syphilis.'. 144 

44. Syphilis of the shaft of the humerus. 145 

45. Paget’s deforming osteomyelitis (Stanford Clinic Case No. 1). 148 

46. Paget's deforming osteomyelitis (Stanford Clinic Case No. 2). 149 

47. Paget’s deforming osteomyelitis (Dr. Ethan Smith's patient). 150 

48. Paget’s deforming osteomyelitis, skiagram of the skull. 151 

49. Paget’s deforming osteomyelitis, skiagram of bones of the legs. 152 

50. Paget’s deforming osteomyelitis (Dr. Ethan H. Smith’s second case) 153 

51. Distal two-thirds of femur and proximal end of Dr. Smith's second 

case sawn sagittally. 154 

52. Rickets, low-power photomicrograph of the costochondral junction. . 159 

53. Skeleton of rickety child. 160 

54. Rickets . 162 

55. Rickets, skiagram of a knee. 164 

56. Discrete tuberculosis in the bone marrow. 185 

57. Tuberculosis in the bone marrow immediately beneath the articular 

cartilage . 187 

58. Joint tuberculosis, low-power photomicrograph. 188 

59. Tuberculosis of the knee-joint in a child. 189 

60. Tuberculosis of the metacarpal-phalangeal joint. 192 

61. Photomicrograph, low-power, from a case of tuberculous arthritis... 195 

62. Tuberculosis of the head of the radius. 197 

63. Low-power photomicrograph of the central gap shown in preceding 

figure . 198 

64. Synovial tuberculosis, low-power photomicrograph. 199 

65. Low-power photomicrograph of synovial tuberculosis of the rapid 

destructive form. 200 


































ILLUSTRATIONS 


11 


G6. Low-power photomicrograph of an incapsulated old cheesy collection 

dug out from the fibrous adhesions in an ankle-joint. 202 

67. Old calcified tubercle in the bone marrow. 204 

68. Old, well-incapsulated tuberculous focus found immediately beneath 

the joint cartilage. 206 

69. High-power photomicrograph of a portion of the wall of the old 

tuberculous focus shown in preceding illustration. 208 

70. Low-power photomicrograph of a portion of a collection of rice bodies. 209 

71. Photomicrograph of one of the rice bodies shown in the preceding figure 210 

72. High-power photomicrograph of a portion of the rice body shown 

in the preceding figure... 213 

73. Posterior aspect of tuberculous spine of child. 238 

74. Spine shown in preceding figure, laid open from behind. 239 

75. Tuberculosis of the spine. 240 

76. Tuberculosis of the cervico-thoracic spine. 245 

77. Tuberculosis of the lumbar spine. 246 

78. Tuberculosis of the second lumbar vertebra. 247 

79. Incisions for the Hibbs and Albee operations. 254 

80. Tuberculosis of the spine; crushing together of the bodies of the 

third and fourth lumbar.. 256 

81. Antero-posterior view of the preceding.. 258 

82. Specimen removed at necropsy from a case of hepatic cirrhosis. 261 

83. Ordinary plaster jacket. 263 

84. Calot head sling. 264 

85. The “grand"’ Calot jacket. 266 

86. The “grand” Calot jacket, side view. 267 

87. Diagrams showing the effect of fixed adduction and of fixed abduc¬ 

tion upon the attitude of the lower extremity. 275 

88. The short plaster of Paris spica in the treatment of hip-joint tuber¬ 

culosis . 281 

89. The Thomas hip splint. 283 

90. Ordinary old-fashioned hip splint. 285 

91. Incisions for hip-joint resection. 290 

92. The Kocher and the Murphy incisions. 292 

93. Old tuberculosis of the knee-joint. 296 

94. The Thomas knee splint.. 303 

95. The ring of a left Thomas knee splint. 304 

96. Incisions for opening the knee joint. 305 

97. Whitman's incision for excision of the talus. 311 

98. Tuberculosis of the tarsus. 313 

99. Tuberculosis of the calcaneus. 315 

100. Tuberculosis of the wrist. 327 

101. The wrist shown in Fig. 100, eleven months after operation. 328 

102. Author’s operation with bone graft for tuberculosis of the wrist. 329 

103. The Smith-Peterson approach. 333 

104. Flap reflected by subperiosteal dissection from lateral surface of 

the ilium. 333 







































ILLUSTRATIONS 


12 

105. The dotted line represents the sacro-iliac joint projected on the 

lateral surface of the ilium. 334 

106. The dotted line represents the sacro-iliac joint projected on the 

lateral surface of the ilium. Window removed as described for 
cases of osteomyelitis. 334 

107. Window removed from ilium down to the sacro-iliac joint. 335 

108. Cortex removed from portion of the sacrum. 335 

109. The block of bone from the ilium countersunk into the sacrum. 335 

110. Tuberculosis of the metatarso-phalangeal joint. 338 

111. Low-power photomicrograph of the bone at the articular surface.... 357 

112. Distal end of two femora. 366 

113. Photograph of a resected knee from a typical case of chronic arthritis 368 

114. Chronic arthritis of the great second type. 370 

115. Sections of head of femur from a case of second-type arthritis. 371 

116. Photograph of a stained slide from section A of the preceding. 372 

117. Photographs of stained slides from sections taken a short distance 

from each other from the head of the femur. 373 

118. Section through the neck of the femur. 374 

119. Photograph of stained slide of a section of the head of the femur. . . . 375 

120. Photograph of stained slide from a case of second-type arthritis of 

the knee. 376 

121. Eburnated bone at tlie articular surface. 377 

122. Low-power photomicrograph of articular cartilage. 378 

123. Typical appearance of cartilage from a second-type arthritis of 

the hip. 379 

124. Rather high-power photomicrograph of some of the cartilage tatters. 380 

125. Cellular infiltration in the marrow. 381 

126. Low-power photomicrograph of a section of the synovial membrane. 382 

127. Articular surface of head of femur. 384 

128. Chronic arthritis of the great second type. 385 

129. Chronic arthritis of the second type involving the thoracic spine. 387 

130. The same patient as shown in the preceding figure. 388 

131. Legg's disease. 404 

132. Legg’s disease. 406 

133. Legg’s disease. 407 

134. Joint mice in the elbow. 410 

135. Two joint mice removed, exact size, from elbow shown in Fig. 134.. . 411 

136. Photograph of a section of the larger of the mice shown in the pre¬ 

ceding figure. 412 

137. Low-power photograph of the smaller of the joint mice. 413 

138. Loose body removed from joint, natural size. 414 

139. Rbntgenogram showing defect in surface of condyle of femur. 415 

140. Typical joint mouse from medial condyle of the knee. 416 

141. Low-power photomicrograph of the marked portion of the preceding 416 

142. Osgood-Schlatter disease. 421 

143. Osgood-Schlatter disease. 422 

144. Osgood-Schlatter disease. 423 



































SECTION I. 

GENERAL CONSIDERATIONS 








INFLAMMATION IN 
BONES AND JOINTS 


CHAPTER I. 

GENERAL CONSIDERATIONS. 

Disease in bone derives its special interest from the 
tact that it runs its course locked up in a narrow case or 
shell which influences its manifestations and treatment. 
Diseases of the small bones of the extremities, and of the 
ends of the long bones, are peculiar also in that they have 
in their immediate vicinity a closed cavity, the joint, whose 
involvement often overshadows the disease in the bone, and 
gives the clinical picture its stamp. 

In our studies six tissues require examination: (1) 
Bone tissue proper, (2) Marrow, (3) Periosteum, (4) 
Cartilage, (5) Synovial membrane, (6) Ligament. In¬ 
asmuch as difference of opinion often springs from differ¬ 
ence of definition, we shall define these terms as well as 
describe the tissues they represent. 

Bone is an animal substance composed of organic ma¬ 
terial impregnated with salts of lime and magnesium. * 1 
Bone cells also are an integral constituent. Bone is 
divided into two classes: dense, and spongy or cancellous, 

but the bone in each is the same, and only differs in its 

* «/ 

arrangement and in its amount. 

Dense bone is found at the circumference of the shafts 
of the long bones, and as a layer on the outside of all spongy 

1 Bone ash consists of calcium phosphate 84 per cent., magnesium phosphate 

1 per cent., other calcium salts 7.5 per cent., carbonic acid 5.5 per cent. 

15 



16 


INFLAMMATION IN BONES AND JOINTS 


bones or portions of bone. Under the articular cartilage 
it is prolonged as a thin layer in the normal state. On 
the inside of the cortex of the shaft it may end abruptly 
or it may be lined by a small amount of spongy bone. The 
second is the more frequent condition. 

As it approaches the end of a long bone the layer of 
dense bone tapers off, to be prolonged under the cartilage. 



Fig. 1.—Slice of the distal portion of the normal human femur. Note the spongy bone on 

the inside of the cortex. 


The inside of the cortex presents no analogue to the 
periosteum on the outside. There is no such structure as 
an “ endosteum.” Endosteum is simply marrow. 

Except under the cartilage the dense bone of the cortex 
is perforated by canals which transport blood vessels. 
Fibres of the periosteum also pass into it. In other words 
the inside of the bone is only relatively a closed cavity. 

Spongy or cancellous bone makes up the bulk of the 
ends of the long bones, and the bulk of the short and the 







17 


GENERAL CONSIDERATIONS 

flat bones, the vertebrae, the sternum, the ribs, carpus, 
tarsus, etc. 

Bone tissue itself is not subject to inflammation, nor 
actively to disease, and simply reacts to disease or change 
in its contained marrow. Usually a mild irritation in 
the marrow causes an hypertrophy of the hone, a stronger 
irritation an atrophy. If the irritation in the marrow be 



Fig. 2.—Low power photomicrograph showing blood vessel entering the bone cortex. Note 

absence of any such thing as endosteum. 


very severe, the bone dies. We are accustomed to speak 
of diseases of bone. It would be more accurate to speak 
of diseases in bone. 

Constant change is going on in the bone, that is, its 
structure is always changing to adapt itself to the uses to 
which it is put. If a part he put at rest, its bony structure 
atrophies, if much work is demanded the hone hypertro¬ 
phies, but both processes are purely passive and are accom- 
* 


2 





18 INFLAMMATION IN BONES AND JOINTS 

plished by the blood vessels in the marrow and in the 
periosteum. 

Done has two great functions. The first is its 
mechanical function as the framework of the body. This 
interests us especially in our study of deformities and of 
fractures. The second is as the container of the marrow. 
This is important in its relation to infection. 

Bone can be injured in only two ways. It can be 
attacked, as we shall see, by disease in its contained marrow, 
or it can be fractured. It cannot be sprained, strained, 
or suffer contusion. This seems self-evident, and yet one 
often hears bone disease ascribed to the late effects of a 
bone injury, other than fracture. Such a thing is of 
course impossible. 

Marrow is the soft tissue within the bone—all the 
soft tissue within the bone. Its situation, not its composi¬ 
tion, determines its name. Wherever there is bone there 
is marrow, in the central canal and in the spongy bone, and 
even, to a small extent, in the dense bone itself. Tissue 
with all the characteristics of marrow is occasionally seen 
in the region of the joints, on the outside of the cortex, 
immediately under the fibrous periosteum. 

Human marrow is of three kinds; first, red or cellular 
or lymphoid; second, yellow or fatty; and third, myxoma¬ 
tous or fibrous. The structure of marrow is so diverse and 
changeable that it is often difficult to say what is normal 
and what is not. Marrow consists of a reticulum of connec¬ 
tive tissue, blood vessels, blood spaces or channels; fat, and 
a greater or smaller number of many kinds of cells. The 
proportion of fat and of these diverse cells determines the 
quality of the marrow, whether it is fatty or lymphoid. 
In myxomatous or fibrous marrow little is present but 
fibrous tissue. 


GENERAL CONSIDERATIONS 


19 


The composition of marrow varies not only in health 
and disease, but also with age . 2 In the human infant 
practically all marrow is lymphoid. In childhood the 
lymphoid marrow gradually disappears from the shafts, 
and then slowly with the lapse of years from the ends of 
the bones also. The adult has little lymphoid marrow 



Fig. 3.—Marrow pocket on the outside of the cortex. Low power photomicrograph. 


in his long bones. It persists longer in the bodies of the 
vertebrae. 

In studying diseases in bone, the changes in the bone 
tissue itself first attract our attention, but give us very 
little information. Whether we examine the bone with 
the naked eye, with the microscope or with the Rontgen 

2 Dickson, W. E. Carnegie: “The Bone Marrow.” London, Longmans, 
Green & Co. ]908. 





20 


INFLAMMATION IN BONES AND JOINTS 


rays we observe that the changes in it are of the simplest 
kind, and are only three in number,—absorption or atrophy, 
production or hypertrophy, and death or necrosis. The 
farther we investigate, the stronger grows our conviction 
that all changes of bone tissue are purely passive, :: and 
are simply the result of changes in the contained marrow. 

The marrow is one of the most complex, changeable, 
active and interesting tissues of the body, and reacts quite 
promptly to most infections. Fraenkel 3 4 found typhoid 
bacilli in the bone marrow of every one of 110 patients 
dying of typhoid. Areas of necrosis in the marrow are 
frequently observed in autopsies of patients who have died 
of infectious diseases. 

In laboratory animals dying of an infection, I have 
often noticed a marked engorgement of the marrow; so 
often that I have come to regard it as a pathognomonic sign 
of an infection. Probably the “aching bones” at the be- 
ginning of an infectious disease are due to this congestion. 

As we shall see later, the marrow in tuberculosis shows 

. w ***•:■• - •*.- ‘ ■ ■ « . 

typical tubercles, in suppurative osteomyelitis, engorge¬ 
ment, pus cells, colonies of bacteria, etc., in chronic bone 
disease the fibrous changes later to be described. 

The theory of the purely passive role of the bone tis¬ 
sue itself is not by any means generally accepted. In fact, 
it must be said that by far the weight of opinion lies on 
the other side. Most writers believe that the bone tissue 
itself is capable of active inflammation, and attempt to 
differentiate ostitis from osteomyelitis. In the same way 
the differentiation is made between periostitis and inflam¬ 
mation of the marrow (or bone) immediately below the 

3 Klemm, P.: “ Die Osteomyelitis des Kindesalters.” Berlin, 1914. S. Karger. 

4 Fraenkel, Eug.: “ Ueber Knochenmark und Infektionskrankheiten,” 
Mtinchener medicinische Wochenschrift, 1920, xlix, 561. 




GENERAL CONSIDERATIONS 


21 


periosteum. Klemm, in his book on osteomyelitis, discards 
completely the terms ostitis and periostitis. Probably the 
periosteum, like any other fibrous tissue is subject to 
inflammation, but I think that the term periostitis as ordi¬ 
narily employed is a misnomer, and that what we know as 
periostitis is really an inflammation of the subjacent bone 



Fig. 4.—Low power photomicrograph of diffuse tuberculosis in the bone marrow. 


marrow. The terms rarefying ostitis and productive ostitis 
are used synonymous with bone absorption and bone 
production, but seem to possess no particular merit. 

The marrow, especially the lymphoid marrow, is to be 
regarded as a chemical laboratory, the bone simply as the 
building which houses it. A knowledge of the composition 
of the marrow gives 11 s a ready comprehension of its vul¬ 
nerability to infections and to their location as well. 


22 


INFLAMMATION IN BONES AND JOINTS 


The marrow of spongy bone, at least well into adult life, 
and in children the marrow of the shafts also, is essentially 
a lymphoid tissue. If pus germs of sufficient virulence are 
carried in the blood stream to a lymph node, the lymph 
node suppurates and breaks down; if they are carried to 
the bone marrow, the bone marrow does the same. The 
difference in the course of the disease in the two cases is, 
in the first place a question of the amount of tissue involved, 
and in the second place one of environment. In osteomye¬ 
litis the products of suppuration are shut up in an almost 
impermeable shell and this fact makes the process much 
more severe, and increases the danger immeasurably. 

This explanation of the frequency of the occurrence of 
infections of the bone marrow in the young is not the 
standard one. Most authorities emphasize the ^etiological 
importance of trauma. Some affirm that rapid growth pre¬ 
disposes to infection. Lexer 5 ascribes to the arrangement 
of the blood vessels about the epiphyseal line, the causal 
role in the frequency of infections near the end of the bone. 
His view might be said to be at present the accepted one. 
The matter will be taken from the realm of speculation 
when the bones are sectioned at necropsy with the same 
thoroughness as the other organs of the body. 

The Periosteum is the tissue which covers the bone 
in all places except those covered by the joint cartilage. 
Its structure and function have been the subject of much 
discussion, into which we shall not enter at any length here. 
The difference of opinion is due partly to a lack of exact 
definition, and partly to faulty reasoning. A knowledge 
of the subject is advisable if one would understand the 
subject of bone formation. 


5 Lexer, E.: “ Weitere Untersuchungen iiber Knochenarterien und ihre 
Bedeutung fur krankhafte Vorgaenge,” Arch. f. klin. Chir., 1904, lxxiii, 481. 



GENERAL CONSIDERATIONS 


23 


If one looks at the periosteum of the shaft of a growing 
hone, that is, of a bone of a child, one will often distinguish 
two layers, an outer or fibrous, and an inner or cellular 
layer. The cells in the latter are probably osteoblasts or 
bone-forming cells, such as are seen on the margin of all 
growing bone; such as are seen on the margin of bone 



Fig. 5. —Low power photomicrograph of normal human bone, 
showing periosteum and fairly dense bone. The section was taken 
of the so-called metaphysis, that is in the region where the dense 
bone is changing to spongy. In this stained slide the bone cells 

appear as small dots. 

trabeculae in the interior, when they are growing in thick¬ 
ness. These cells are described as part of the periosteum, 
but they really are part of the hone, and have nothing 
whatever to do with the periosteum proper. In the speci¬ 
men from an adult this cellular layer may be present 

or absent. 

The periosteum consists of a rather loose-meshed 
fibrous tissue. Here and there this fibrous tissue may he 



24 


INFLAMMATION IN BONES AND JOINTS 


replaced by cartilage, or by fibrocartilage. This is perios¬ 
teum none the less, no matter what its structure. 

Fibres of the periosteum run down into the bone, but, 
of course, as soon as they enter the bone they cease to be 
periosteum, and become marrow. With both marrow and 
periosteum the situation, not the structure, determines 
the name. 

The blood vessels of the periosteum send branches into 
the bone. These run in small canals, and anastomose with 
the vessels of the marrow. 

Ligaments are composed of dense white fibrous tissue, 
and serve to bind the bones of an articulation together. 
Their fibres pass into the articulating bones, but some 
of the more superficial are continuous with the periosteum. 

A Joint is usually a closed cavity between two or 

«/ 

more bones, and is bounded by two tissues, the synovial 
membrane and the cartilage. 

Cartilage consists of cells and basement substance. 
The cells have a definite capsule and a characteristic ap¬ 
pearance which often helps to identify the tissue under 
the microscope. The basement substance consists of col¬ 
lagen fibrils impregnated with chondromucin. Cartilage 
contains according to age 3 to 6 per cent, of mineral sub¬ 
stances, of which calcium sulphate forms from 48 to 92 
per cent. 

The articular cartilage is of the hyaline type. Its 
basement substance appears homogeneous in the normal 
subject, but in certain joint diseases it loses this homogen¬ 
eous appearance and takes on a distinct fibrous structure. 
The fibres run parallel to the surface superficially, but 
deeper in, at right angles to it. This fibrillar appearance 


GENERAL CONSIDERATIONS 


25 



it said to be present also in joints which have been immobil¬ 
ized for any length of time. 

The joint cartilage in the foetus is covered by a perichon¬ 
drium, but in infancy, after function has been established in 
the joint, the perichon¬ 
drium disappears. In 
certain diseases thereafter 
the superficial portion of 
the cartilage may take on 
the appearance of a peri¬ 
chondrium, especially 
about the margin where it 
shades into the synovial 
membrane, but the normal 
joint cartilage in the adult 
is without perichondrium. 

T li e dense, smooth 
nature of the joint carti¬ 
lage adapts it admirably 
for its functions of motion 

and of weight bearing, p IG . 6.—Photograph of stained slide from a sagittal 

, . n , • section of the knee of a normal dog. 

and these iunctions are 

subserved by tbe absence from it of blood vessels and 


of nerves. 

It is well to remember that in childhood the joint 
cartilage is simply a portion of the cartilaginous epiphysis. 
As time goes on the growth of the bone nucleus separates 
it from the epiphyseal cartilage, until, with the disappeai- 
ance of this, the articular cartilage becomes the sole remnant 
of the mass of hyaline cartilage of which tbe whole bone 
was originally composed. Cartilage may really be viewed 
as essentially an embryonal tissue doomed eventually to 



£6 


INFLAMMATION IN BONES AND JOINTS 


ossification. Some of it ossifies early, some of it late. The 
individual constitution influences the time of ossification, 
as does the manner of life, and possibly, the occupation. 
Viewed in this light the stiffening of the joints as age 
advances, is easily understood. On the other hand some 
persons have supple joints which work smoothly even at 
an advanced age. 

Fibrocartilage is found in the joints in the shape of 
interarticular discs or menisci. They serve to lessen shock 
or to add security. In structure they partake of the nature 
of the ligament and of hyaline cartilage. In the vertebral 
joints they add motion and stability. The joints of the 
vertebral bodies possess no hyaline cartilage, no joint 
cavity and no synovial membrane. 

The articular cartilage possesses no blood vessels. No 
lymph vessels have ever been found in it, though their ex¬ 
istence has been assumed by some authorities. Exactly 
how the cartilage is nourished is not known. It is supposed 
to draw its nourishment from the marrow beneath, and 
possibly from the synovial membrane at its margin. Cer¬ 
tainly its whole reaction to disease seems to depend upon 
the condition of these tissues. It is not subject to inflam¬ 
mation, nor directly to disease. It simply suffers second¬ 
arily from involvement of the synovial membrane and of 
the marrow. Probably there is no such thing as a primary 
disease of the articular cartilage nor invasion of it from the 
joint side; authorities differ on this last point, the majority 
holding the contrary opinion. 

The articular cartilage, and the epiphyseal cartilage 
while it is present, form a barrier to the spread of infection, 
practically an absolute one. The broad general rule may 


GENERAL CONSIDERATIONS 


27 


be laid down that an infectious process can not make its 
way through a cartilage whose nutrition is intact. Hence 
infectious processes in the bone marrow, in order to reach 
the joint, must either travel around the margin of the 
cartilage, or else first shut off its nutrition from beneath, 
and then perforate it. If the view is correct, as I believe it 
is, that the cartilage is immune from invasion from the 



Fig. 7.— Section of dog’s patella, camera lucida drawing. Joint cartilage beiow. Note t^e 
little pouch at either end of the cartilage, lined with synovial membrane, to^allow- for motion. 
Note also the buttress of bone beneath the cartilage, and the absence of any perichondrium. 


joint side, then any infection, to pass from the joint 
to the bone marrow must travel around the margin of 

the cartilage. 

The Synovial Membrane is a connective tissue 
structure which bounds the joint in all places except those 
bounded by the articular cartilage. It covers intra- 
articular ligaments, and, in certain joints, notably the 
knee, is prolonged inward in the form of fringes or curtains. 
It secretes a viscid fluid which lubricates the joint, and 
normally is just sufficient to serve this purpose and no 









28 


INFLAMMATION IN BONES AND JOINTS 


more. The membrane is continuous with that lining cer¬ 
tain of the bursae in the immediate neighborhood of some 
joints, so that disease in one readily spreads to the other. 
There is, of course, no such thing as a hernia of a joint. 

The normal synovial membrane is smooth and shining, 
but in the region of its junction with the cartilage, it is 
thrown into folds, to accommodate it to the movement of 
the bones. Here its cells have much the appearance 
of epithelium. 

The junction of the cartilage and the synovial mem¬ 
brane is not abrupt, but the two tissues shade gradually 
into each other, so that it is not possible to say exactly where 
one stops and the other begins. 

When a joint is immobilized for any reason, the 
synovial membrane encroaches upon the cartilage at its 
periphery, replaces it, so to speak, and extends especially 
over its surface. When motion is restored, provided the 
joint has not been damaged by disease, the cartilage 
extends again at its periphery, and regains its former 
limits. 6 This is probably the cause of the stiffness of joints 
after immobilization. It is doubtful if any adhesions, 
properly speaking, are ever caused in a normal joint 
by immobilization. 

The reaction of the synovial membrane to injury or to 
disease is very interesting. If it be irritated it pours out a 

c Nathan, P. W.: “The joint cartilage in its relation to joint pathology.” 
Am. J. of Orth. Surg. 1909-10, vii, 85. 

Brann, Heixricii: “ Untersuchungen iieber Bander Synovialmembranen 
und Gelenkknorpel.” Dent Zeit. f. Chir., 1894, xxxix, 35. 

Reuber, Carl: “On the cartilages and synovial membranes of the joints,” 
Jour. Anat. and Physiol. 1874, viii, 261. 

Hammar, J. Aug.: “ Ueber den feineren Bail der Gelenke.” Archiv. f. Mik. 
Anat., 1894, xliii, 266, 813. 



GENERAL CONSIDERATIONS 


29 


secretion whose nature depends, of course, upon the irri¬ 
tant. The mere presence of this fluid probably causes 
thickening and inflammation of the membrane. It is thrown 
into folds, and takes on a villous structure. These villi 
may attain great size and number, giving to the inner sur¬ 
face of the joint a marked shaggy appearance. 

No stomata ever have been demonstrated in the mem- 



b r a n e, and the 
method of the subse¬ 
quent exit of the fluid 
from the joint is not 
known. Strange to 
say, fluid does not 
accumulate i n t h e 
joints i n cases o f 
oe d e m a of the 
extremities. 

Any infection of 
the synovial mem- 
brane causes the 
thickening and 
villous condition, and 
the characteristics of 
certain infections are 
beautifully shown in the membrane, as they are in the 

bone marrow. 

The opinion formerly prevailed that the synovial mem¬ 
brane was a closed sac extending out over the cartilage, 


Fig. 8. —Low power photomicrograph, showing typical 
appearance of the synovial membrane in an acute inflam¬ 
mation. This is from a case of probable syphilitic arthritis 
wrongly diagnosed as tuberculosis and infected at oper¬ 
ation. Synovial membrane above. Ligament below. 


but this is not a fact. It is a section of a tube, ending at 
the border of the joint cartilage, with which, as has been 
said, it is continuous. In the embryo, however, and for a 


30 


INFLAMMATION IN BONES AND JOINTS 


while after birth, the synovial membrane is continuous with 
the perichondrium. 

In all joint inflammations the synovial membrane is to 
be regarded as the active tissue, the cartilage as the passive. 
It follows that the terms synovitis and arthritis are 
synonymous. With an arthritis, the adjacent bone marrow 
may or may not be involved; that is, an osteomyelitis may 
or may not be associated with the arthritis. 

We recognize, then, in inflammations of bones and 
joints, only two active tissues; the bone marrow and the 
synovial membrane. The ligament, the cartilage, the bone 
tissue itself, and probably the fibrous periosteum all play 
a purely passive role. We are wont to use the term 
“ periostitis ” quite frequently, but the real inflammation in 
such a case is usually in the bone marrow in the imme¬ 
diate vicinity. 

Broadly speaking the marrow and the synovial mem¬ 
brane are vulnerable to the same infectious agents. Any 
bacteria which invade one can invade the other. However, 
certain infections show a preference for the marrow, cer¬ 
tain for the synovial membrane, while certain others affect 
both tissues without preference. A knowledge of this fact 
helps us in our diagnosis. Thus treponema pallidum 
belongs in the first class, the gonococcus in the second, and 
the tubercle bacillus in the third. 

We note also that while some infections always start in 
the lymphoid marrow, and practically always remain there, 
others start in either the lymphoid or the fatty marrow, 
with about equal frequency. The lymphoid marrow in the 
ends of the long bones seems to be the great chemical lab¬ 
oratory in which most infections germinate; that in the 


GENERAL CONSIDERATIONS 


31 


short bones to a lesser degree. We shall see how they may 
never travel beyond the limits of this tissue in certain 
instances. Indeed, as in the lungs, only the necropsy may 
reveal that they have ever been present at all. In most 
eases, however, they show a tendency to spread. 

The direction in which the various infections spread is 
also a matter of interest, and often an aid in diagnosis. 
Tuberculosis always travels toward the joint if it travels 
at all. Pus infections usually travel toward the shaft, less 
often towards the joint, but streptococcic infections show 
the contrary tendency, and travel toward the joint. 

Fundamentally the pathological characteristics of all 
bacterial bone and joint infections are the same, as are the 
characteristics of flowers or of trees. We distinguish 
among them by their minor traits. One great difference 
exists between the botanist’s task and ours. He has his 
object exposed to his senses, while ours is covered by the 
skin and subcutaneous tissues. Not until we have a culture 
of the offending organism are we sure of its identity, but 
the more carefully we study its habits, its life history, so to 
speak, and its effects, the more often shall we be able to 
recognize it well enough for all practical purposes, and to 
institute our measures of cure, without waiting for a posi¬ 
tive identification. On the other hand, remembering the 
impossibility of reaching a positive conclusion without the 
aid of the microscope, we do not overestimate our diagnos¬ 
tic ability, and consequently do not so often make humili¬ 
ating mistakes. 


32 


INFLAMMATION IN BONES AND JOINTS 
THE FORMATION OF BONE, * * * * 8 * > 10 * > 12 * * ’ 1S 


The phenomena of bone production have been known 
for a long time, but the identity of the active agents of the 
process, and their exact role, are still a subject of discussion. 

Until comparatively recently the “ metablastic ” theory 
of bone formation prevailed. According to this the various 
members of the connective tissue group possessed the 
power in certain circumstances of changing to one another. 
This theory is at present not widely held. It has generally 
been displaced by the “ neoblastic ” theory, which predi¬ 
cates the existence of a definite bone-forming cell, 
or “ osteoblast.” 

The exact identity of the osteoblast is not known. It 
is described as a small, round or polyhedral cell, with 
sharply staining nucleus, usually seen on the borders of the 
trabecula? or on the outside of the cortex, but without 
characteristics clearly enough defined to permit its identi¬ 
fication away from its accustomed habitat. We see these 
cells in great numbers on the outside of young growing 
bone, and on the edge of the trabecula* when we believe that 
bone is being built up, and we are wont to conclude, there- 

7 Arey, L.: “The Origin, Growth and Fate of Osteoblasts,” Amer. J. of 

Anatomy, 1920, xxvi, 315. 

8 Todd, T. W.: “Development and Growth of Bone,” Journal of Anatomy 

and Physiology, 1912-1913, xlvii, 177. 

8 Buscii : “ Die Osteoblastheorie auf normalen und pathologischen Gebiete,” 

Deutsche Zeitschrift fiir Chirurgie, 1878, x, 59. 

10 Bilroth : “Anatomische Beobachtungungen iiber das normale Knochen- 
wachsthum,” Archiv fiir klinische Chirurgie, 1864, vi, 712; “ Ueber Knochen- 

resorption,” Archiv fiir klinische Chirurgie, 1862, ii, 118. 

11 Meyer, Arthur: “Side Lights on Multiple Myeloma.” American Journal 
of Medical Sciences, 1918, clvi, 329. 

12 Ely, Leonard W.: “The Formation of Bone,” Ann. of Surg., 1919 

lxix, 225. 

13 Leser, Edmund: “Ueber die histologischen Vorgaenge auf der Ossifi¬ 
cations Grenze,” Archiv f. klinische Chir., 188, xxxvii, 511. 





GENERAL CONSIDERATIONS 33 

fore, when we see these small cells in this situation that bone 
formation is going forward. This is not always true. The 
borders of the trabecula? often present the same appear¬ 
ance when we know quite well that the bone is being torn 
down. This has led some observers to the conclusion that 



Fig. 9.—Low power photomicrograph from a case of marrow tuberculosis. The bone is being 
torn down, not built up, but the edges of the trabeculae are covered with cells corresponding to 
the ordinary description of osteoblasts. Note the interval between these cells and the trabecula. 


the same cell which builds hone up, can also tear it down, 
that is, that the osteoblast is the same as the osteoclast. In 
this view I am inclined to concur. I have in my possession 
stained slides of marrow of tuberculosis and of acute 
osteomyelitis, in which all the evidence points to hone 
absorption, but in which cells with the typical appearance 






34 


INFLAMMATION IN BONES AND JOINTS 


of osteoblasts are seen in great numbers on the borders of 
the trabecula?. 

The prevailing view is that the osteoclast is a large cell 
—a giant cell—seen usually in an excavation on the border 
of the trabecula (Howship’s lacuna) or at a short distance 
from it. Some observers believe that this giant cell is the 



Fig. 10.—High power photomicrograph of a portion of the preceding slide. 

result of the bone absorption, and not its cause. Bone 
probably can be absorbed without the agency of any special 
cell, by simple absorption of its lime salts—“ halisteresis.” 

Whence comes the osteoclast, if there be such a cell, is 
not known. The origin of the osteoblast is still unsettled. 
Geddes 14 says it wanders in from the epiblast, but it is 
generally considered a mesoblastic cell. Some say that it 

14 Geddes, A. C.: “Origin of the Osteoblast and Osteoclast,” Journal of 
Anatomy and Physiology, 1912, xlvii, 159. 







GENERAL CONSIDERATIONS 35 

is brought by the blood stream, but Moschcowitz 15 says 
that it is simply a mesothelial cell arising in the process of 
angiogenesis. Lie says that the endothelial cell in the vessel 
wall, the osteoblast, the osteoclast and the bone cell are all 
fundamentally the same, with the same potentialities. 



Fig. 11. — Low power photomicrograph from a case of acute suppurative arthritis. T, tra¬ 
becula, M, marrow. Most of the trabecula is dead, but its upper left, and its lower right 
hand border show signs of a deposit of new bone. The bone cells here stain. The marrow is 
the seat of an intense inflammation. At R appears what is known as rarefying osteitis. 


What function they eventually possess simply depends 
upon their surroundings. 

Stained slides from specimens of fractures or resec¬ 
tions, or from the inside of the cortex of growing bone, where 
nature is rearranging the architecture of the bone, show 
the classical giant cell osteoclast in great numbers. When, 

15 Moschcowitz, Eli: “The Relation of Angiogenesis to Ossification,” 
Johns Hopkins Hospital Bulletin, 1916, xxvii, 71. 




36 


INFLAMMATION IN BONES AND JOINTS 


however, the bone is being absorbed as the result of an 
infectious process in the marrow, or after being buried 
experimentally in the soft tissues, these giant cell osteo¬ 
clasts are few in number or are absent altogether. 

If the neoblastic theory is correct, as we shall assume 
that it is, then three things are necessary for bone forma¬ 
tion, and these are: first, the active agent, the builder; 
second, the building material; and third, the stimulus. 

Ollier, 16 in 1867, first described a “ cambium ” layer of 
the periosteum and ascribed to it a bone forming function. 
The question was debated for years, until finally the 
periosteum came to be regarded as the great active agent in 
bone formation. In 1912 MacEwen 17 denied this func¬ 
tion, and affirmed that the periosteum was simply a limiting 
membrane and that the marrow formed bone. The question 
is still being debated, and much experimental and clinical 
evidence has been adduced on both sides. 18 Without going 
into the details of the controversy, let us assemble the 
known facts concerning bone formation, and see if we can¬ 
not reach a satisfactory conclusion and one that will be of 
practical service. Manifestly we cannot throw out the 
evidence submitted by reliable observers, and yet we cannot 
accept conclusions diametrically opposed. The chief diffi¬ 
culty disappears when we remember that neither the 
periosteum nor the marrow forms bone, but the osteoblast. 

16 Ollier: “ Le Regeneration des Os,” 1867, v, Masson et fils, Paris. 

17 Mac Ewen, William: “Growth of Bone, The,” 1912, Maclehose and Sons, 
Glasgow. The Macmillian Co., New York. 1912. 

18 Hass, S. L.: “Regeneration of bone from periosteum,” Sure/. Gyn. and 
Obst., 1913, xvii, 174. 

Jokoi: “ Experimented Beitrag zur Knochenneubildung durch Injections 
bez. Implantation von Periostemulsion,” Deutsche Zeitschrift fur Chirurgie, 
1912, cxviii, 433. 




GENERAL CONSIDERATIONS 


37 


The following statements will hardly meet with 
opposition: 

1. Intracartilaginous bone formation begins with the 
pushing of blood vessels into the cylinder of cartilage in a 
long bone. Around these blood vessels calcification and 
ossification take place. A similar process takes place later 



F ig . 12.—The blood vessel has pushed its way into the epiphyseal cartilage, and has initiate 
bone formation in the centre of ossification. Low power photomicrograph itom the knee 
joint of a foetus at term. New bone in upper left hand corner. 


in the epiphysis. This is hone formation without marrow 
or periosteum. 

2. Bone is formed in the walls of the aorta, and in the 
kidneys of laboratory animals whose renal vessels have 
been tied off. 19 Again bone formation without marrow 

or periosteum. 

3. Bone is formed from cartilage or from fibrous 

19 I.iek : “ 7,ur Frage der heteroplastischen Knochenbildung," Archm 

fiir klinische Chiruvgie, 1906, lxxx, 2/8. 














38 


INFLAMMATION IN BONES AND JOINTS 


tissue, in the marrow of adult bones, without the aid of 
the periosteum. 

4. Bone is formed in fibrous tissue—intramembranous 
bone formation—before any marrow is present. 



Fig. 13.—Low power photomicrograph of early stage of intracartilaginous bone formation. 

Blood vessels pushing their way into the cartilage. 

5. Bone is formed on the outside of the cortex, beneath 
the periosteum, again bone formation without marrow. 

6. New bone is sometimes formed in necrotic or hyaline 
tissue, e.g. y lymph nodes, tuberculous foci, corpora albi- 
cantia, thickened pleura?, etc., etc. 

7. Buried bone contacted with other bone and enjoying 
a functional use, persists and is renewed. Bone buried in 
the soft tissues, without function, slowly disappears. 





GENERAL CONSIDERATIONS 


39 


8. Bone is never formed except in the presence of 
blood vessels. The entrance of blood vessels into a tissue 
to be ossified is the first step in the process. 

If we sum up our facts we find that three things are 
necessary for bone formation: 

1. Blood vessels—the builder. 

2. Either (a) a loose meshed fibrous tissue, or (h) a 
homogeneous (cartilaginous matrix), or a granular or a 
necrotic material—the building material. 

3. A stimulus, physiological or pathological as the case 
may be. It is this stimulus which causes the blood vessels 
to push into the cylinder of cartilage in the first place, and 
which causes the bone production in the aorta, for instance. 
We recognize function as a stimulus, and the mere presence 
of bone as another. 

It is therefore seen that neither periosteum nor marrow 
is essential for bone production, and that neither of them 
forms bone, in the proper meaning of the word. In each 
tissue we simply conclude that the conditions are suitable 
for bone production. The materials are there, and given 
the stimulus, physiological or pathological, bone will be 
manufactured out of the fibrous or cartilaginous tissue in 
the periosteum or marrow. The true marrow cells, the 
characteristic marrow cells, the cells which give the marrow 
its stamp and its function, probably have no role whatever 
in bone building. 

We observe other phenomena in the formation of bone, 
which are of use to us in our clinical work: 

Cavities in bone are filled up to the old level, in the 
absence of infection. Normally the new bone will not go 
beyond the old level. The shape of the cavity does not 
materially influence this process. In the presence of a 
pus infection the shape of the cavity does influence it. 



40 INFLAMMATION IN BONES AND JOINTS 

In such a case steep walled cavities will not fill in. The 
walls must be beveled oft before healing will take place. 

It is doubtful if nature ever fills up with new bone the 
cavities in bone caused by certain old closed chronic infec- 
tions. Old cheesy tuberculous foci may persist for years. 
They may show calcification but not ossification. They do 
not become vascularized. Old bone cysts may persist 
indefinitely. On the other hand, bone destroyed by a syph¬ 
ilitic process, can probably be restored by nature without 
artificial aid. 

The examination of old specimens of buried bone 
teaches us that sterile dead bone, under the stimulus of 
function, is replaced by nature. She employs the old bone 
as a scaffold. The details of this will be set forth under the 
bead of bone transplantation. 

Bone cannot grow out any distance from its own 
level, unless it have a bridge or scaffold on which to grow. 
If the bead of the femur be cut off, a new bead will not 
grow on the neck. If the shaft of the tibia be removed for 
the cure of a suppurative osteomyelitis, new bone grows 
out for a very short distance from the pieces of bone left 
behind, and then stops. Nature perhaps uses the perios¬ 
teum as a scaffold and builds bone along it to connect up 
the fragments. 

It may be laid down as a general rule that in bone, as in 
other tissues, a mild irritation, especially an intermittent 
one, causes an hypertrophy, a severe one, an atrophy. If 
the irritation be very severe, the bone dies—necrosis. 
Whatever the ultimate cause of the process may be, the 
immediate cause of the hypertrophy, the atrophy or the 
necrosis is to be sought, in the interior of the bone in the 
vessels of the hone marrow, at the surface in the vessels of 
the periosteum, and of the superficial cortical marrow. 



GENERAL CONSIDERATIONS 


41 


Halisteresis. —Formerly the view was widely held that 
hone could be removed by the action of some ferment which 
first dissolved the lime salts without the medium of any 
special bone destroying cell, any osteoclast. One sees this 
view seldom now-a-days in American text-hooks, but there 
is much evidence to support it, and I believe it is true, in 
many instances, possibly in all. 20 In sections from malig¬ 
nant growths in bone, this halisteresis is often evident. 

The dense bone of the shaft has less marrow apd fewer 
blood vessels than has the spongy bone, and therefore we 
should expect to see it in less activity both in destruction 
and repair, than in the spongy hone or in the central marrow 
canal. In point of fact all the activity in the process of 
repair after a fracture, is observed at the surface of the 
cortex, as will appear hereafter. 

THE HEALING OF FRACTURES 

If a hole he bored through the cortex, new bone is not 
built straight across the gap, but bone trabeculae, springing 
from the inner aspect of the cortex, form in the marrow of 
the central canal. These slowly increase in number and in 
thickness until they plug up the hole and extend up into it. 
This is the so-called “ internal callus.” To a lesser extent 
the same process takes place on the outside of the cortex. 
Bone trabecuke spring from the exterior surface of the 
cortex, bridge the gap on the outside, extend down into the 
gap, and meet those coming up from the marrow. The 
resulting callus is beautifull y likened by Nichols,- 1 of 

30 Kaufman x, Edward: “Lehrbuch der speziellen pathologischen Anatomie, ’ 
Berlin, G. Reimer, 1917. 

21 The late Doctor Edward Hall Nichols had a most remarkable series of 
slides showing this process, and to him T am indebted for my knowledge of it. 
Tn his death the medical profession suffered an irreparable loss. 







42 


INFLAMMATION IN BONES AND JOINTS 


Boston, to a collar button, which it strongly resembles in 
its shape. 

It is probable that, after a fracture, if the fragments 
could he brought into accurate apposition and could he held 
in absolute immobility, this same collar button would form, 
with a small head and base, and with an infinitely slender 
shank. In practice, however, this is not what we find. The 
continuity of the marrow is broken as well as that of the 
cortex. Nature seems to find great difficulty in building 
bone across the smallest gap, unless she have a scaffold or 
bridge on which to build it. She builds this bridge in the 
following manner: 

Immediately after a fracture hemorrhage takes place 
into the marrow canal and on the outside of the cortex 
beneath the periosteum, which has already been stripped 
from the cortex by the fracture to a greater or less extent. 
The hemorrhagic exudate on the outside of the cortex is 
replaced by granulation tissue, and this in turn by fibrous 
tissue and cartilage. As time goes on then the cartilage is 
ossified by penetration of blood vessels. The greatest activ¬ 
ity in this process is seen to be manifested on the external 
aspect of the cortex, and especially in the angle between 
the cortex and the periosteum. I have watched this process 
taking place in three series of experimental fractures on 
cats, and in no instance have I been able to detect any evi- 
dence that the periosteum takes an active part in it. The 
sole function of the periosteum is to hold the soft callus 
firmly against the bone until cartilage has formed in it. 

This external callus is the chief means of joining the 
two bones together and may be compared to the “ wiped 
joint ” with which the plumber solders together two pipes. 
It holds the bone ends absolutely immobile until the union 

9 / 

is complete, and until the external surface of the cortex of 


GENERAL CONSIDERATIONS 


43 


one fragment is firmly united to that of the other. It prob¬ 
ably takes about a year for the fractured fragments to be 
united directly, and for the normal bone architecture to be 
restored. Then, if the apposition have been absolutely 
exact, the callus presumably is removed entirely. The 
apposition probably never is absolutely exact; hence some 



p IG |4 _Low power photomicrograph from a stained slide taken from a section °f the out¬ 

side of the coX of the tibia of a dog. The knee joint in the.immediate^vicinity'had been 
resected fourteen days previously. Note the new trabeculae, T, T, T, T, forming on the outside 

of the cortex under the periosteum. 


of the callus always remains, and betrays the site of 


the fracture. 

The formation of this external callus may be seen in 
laboratory animals, and its development may be watched 
also with the Kontgen rays. The bone fragments are seen 
to be united by a firm bony bridge long before there is any 
evidence of union between the ends of the cortices. This 








44 


INFLAMMATION IN BONES AND JOINTS 


K. 4 

mfc'r' 

, A ■' 

■Ki 


direct cortical union probably does not take place for about 
a year. 

The so-called internal callus, so prominent when a hole 
is bored in the cortex of a laboratory animal, plays an insig¬ 
nificant role in the healing of an actual fracture. In my 

experimental fractures it was 
usually rudimentary, and 
never bridged any gap be¬ 
tween the two fragments. It 
certainly does not show in the 
;rjp :#!!M X-ray plate. The bridge of 

bone from the external sur¬ 
face of the cortex of one 
fragment to that of the other 
seems to be the essential feat¬ 
ure of the union. Where for 

any reason it does not form 
•/ 

non-union is wont to result. 

Nature seems to inaugu¬ 
rate two distinct and opposite 
processes after a fracture. 

Fig. 15.—Photograph of a stained slide from With one hand she starts to 
a sagittal section of the knee of a dog. The 

knee had been resected seventeen days pre- build a boiiy bridge Under the 
viouslv. Large pieces of bone had been J © 

removed. 


f. A f ' 7j 


v* 






- 


iff 


periosteum and in the mar¬ 
row, as described, with the other she tries to construct a 
joint. If one looks through the microscope at the ends of 
the bones of a laboratory animal some days after the 
production of a simple fracture, one sees that they are 
separated rather than joined by fibrous tissue which streams 
out from the marrow canal to the periosteum. 

The same thing is seen after experimental resection of 



GENERAL CONSIDERATIONS 


45 


the dog's knee joint . 22 If non-union result, this fibrous 
tissue becomes greatly thickened, and increases in amount. 
Some of it runs across from side to side, some of it between 
the marrow and the periosteum. Cartilage cells often 
appear in it, and almost invariably clefts, which may or 
may not be lined with a syno¬ 
vial membrane. Eventually 
a new joint is established at 
the site of the resection, a 
new joint which bears a 
striking resemblance to that 
seen at the site of an old un¬ 
united fracture. 

In the great majority of 
these experimental resec¬ 
tions a new joint is formed. 

Bony ankylosis is extremely 
hard to secure. The exact 
reverse prevails after sim¬ 
ple fractures in laboratory 

animals. Bony ankylosis is 

*/ *• 

almost invariable, but bony 
union is very rare if the 
periosteum be divided circu¬ 
larly. If the periosteum be 
simply slit before the bone is fractured, union may or may 
not take place. 

Non-union is very rarely seen in the child, in whom new 
bone formation under the periosteum is very active. It is 
said to occur often in certain constitutional diseases, notably 
syphilis. A favorite site of bone syphilis is immediately 
under the periosteum. Impacted fractures almost invari- 

22 Ely, Leonard W.: “Experimental resection of the dog’s knee joint,” 
Annals of Surgery, 1919, lxx, 586. 



Fig. 16. —Photograph of stained slide from 
sagittal section of knee of dog, resected 374 
days previously. Small pieces of bone had 
been removed, 6 mm. from condyles of femur, 
4 mm. from head of tibia. Fibrous union with 
many small clefts in the fibrous tissue. 










46 


INFLAMMATION IN BONES AND JOINTS 



ably unite firmly if they are left alone. Non-union is 
notoriously frequent in portions of bone not provided with 
periosteum, such as the carpal bones and the head of the 
femur and the head of the radius. Lack of contact between 
the fragments tends to prevent union, as does the inter- 
position of soft tissue. 

Weighing all the evidence, clinical and experimental, 

we reach the following 
conclusions: 

If the two fragments of 
a fractured bone not cov¬ 
ered by periosteum can be 
brought into exact apposi¬ 
tion, and can be held firmly 
together without motion, 
they will unite directly after 
a long time. If they be not 
held close together, or if any 
motion take place, a new 
joint probably will be 
formed. 

The role of the perios- 
_ , teum in the healing of frac- 

Fig. 17.—Photograph of stained slide of sagittal tures is to hold the soft 

section of knee of dog, resected twenty-seven 

days previously. Small pieces of bone have been C alluS against tile Olltside 

removed. The end of the femur had been sawn “ 

convex antero-posteriorly and the end of the n -p 4-Up p ni ,r pY 

tibia concave antero-posteriorly. The bones tilt LUI Lca. VY Iieie tUe 

are tightly united by fibrous tissue, • . . 

periosteum is absent or 
divided, non-union is wont to occur. 

Various other reasons have been advanced for the 
occurrence of non-union, notably deficient blood supply 
and alcoholism. 

The opinion is quite widespread that fractures fail to 


GENERAL CONSIDERATIONS 


47 


unite much more frequently than formerly, and for this the 
llontgen rays have been held responsible. The work of 
Albee and Morrison 23 tends to disprove this. They found 
that exposure to the llontgen rays did not retard the 
process of union after experimental fracture of rabbit’s 



Fig. 18.—Photograph of a stained slide from a sagittal section 
of the knee of a dog, resected 150 days previously. Xote the 
absence of bony union. The union is fibrous and in the fibrous 

union are large clefts. 

bones. On the other hand, non-union is extremely rare in 
animals under any conditions. I have seen it only once in 
a simple fracture, but have produced it in two out of foui 
open operations on cats, in which I divided the periosteum 
completely, and fractured the humerus. In anothei senes 
of simple fractures, union v r as almost invariable, if the 

» Albee and Morrison: “Studies in bone growth: an experimental attempt 
to produce pseudarthrosis,” Amer. Jour. Med. Sciences, 1920, clix, 40. 








48 


INFLAMMATION IN BONES AND JOINTS 


animals were permitted to live long enough for the ordi¬ 
nary fracture to united 4 

Besides the changes at the site of a false joint set forth 
above, there are others even more important from a clinical 
standpoint. If the bone ends are exposed to pressure, as 


in the tibia after a simple 
fracture, new bone often is 



Fig. 19. —Photograph of a stained slide from a 
saggittal section of the knee of a dog. The 
knee had been resected 790 days previously. 
Moderately large pieces had been removed 
from the bone ends, and the ends were shaped 
in mortise fashion. Note that the bones are 
separated by a band of fibrous tissue, in which 
is a large cleft. 


laid down at their periphery, 
so that they become broad¬ 
ened, like the ordinary epi¬ 
physis of a long bone. All 
the elements of a permanent 
joint are then present, in¬ 
cluding fibrocartilage over 
the bone ends, and a svnovial 
membrane. The fibrous tis¬ 
sue between the two bones is 
dense and is incapable of 
conversion into bone. It sep- 
a r a t e s the two marrow 
canals. It replaces the peri¬ 
osteum. Frequently also one 
or both marrow canals are 
shut off by a layer of bone, 
from this fibrous tissue. 


Without artificial assistance no union is possible. 

In other instances, especially after compound fracture, 
more or less absorption of the bone ends takes place. They 
become conical, very dense and hard, “ eburnated,” and 

24 Three series of operations were clone. In the first the fracture was a 
simple one, by direct violence: In the second, the periosteum was slit long¬ 
itudinally, and the bone was divided with Liston forceps: In the third, every 
effort was made to sever the periosteum in continuity, before the bone was 
divided. Archives of Surgery, 1922, v. 527. 






GENERAL CONSIDERATIONS 49 

contain little soft tissue except a few blood vessels. Their 
ends are bound together with dense fibrous tissue. Two 
bones whose ends are eburnated will never unite, as wit¬ 
ness the great second type of chronic arthritis. 

For the treatment of non-union, or pseudarthrosis, 
many expedients have been recommended. Among these 
may be mentioned massage, 
tapping the fragments with a 
hammer, setons, counter-irri¬ 
tation, weight bearing, rub¬ 
bing the ends of the bones 
together, perforating them 
with a drill, wiring, plating 
and doweling. The last four 
expedients are still employed. 

The bone dowel has many 
advocates, and doubtless will 
continue to be employed in 
special cases, but otherwise 
the inlay bone graft bids fair 
to displace other means of 
treatment in the ordinary 
case of ununited fracture. It 
possesses the one great ad¬ 
vantage that it is a nor¬ 
mal tissue in its physiological place. The dowel is inserted 
into the marrow canal, where it does not belong, displaces 
its volume of marrow tissue, and probably must be 
eventually absorbed. 

BONE TRANSPLANTATION 

The subject of bone transplantation is an interesting 
one, and has attracted much attention. The discussion, 



Fig. 20. —Photograph, of stained slide from 
sagittal section of knee of dog, resected 922 
days previously. Large pieces of bone had 
been removed. Bony union. 


4 


50 


INFLAMMATION IN BONES AND JOINTS 



at first more or less academic, recently with the develop¬ 
ment of the operative treatment of fresh fractures and 
of ununited fractures, has attained a very real and 
practical importance. Difference of opinion as to details 
still exists, and if one would employ the treatment intelli¬ 
gently, one would do 
well to possess oneself 
of a knowledge of the 
general principles 
governing its use. 

Two things are 
well settled and we 
shall mention them 
before proceeding 
with the discussion: 
1, Live bone from 
another animal, or 
from another person, 
should never be used. 
It will practically 
always result in fail¬ 
ure; 2, In the pres¬ 
ence of suppuration, 
the transplant will al¬ 
most always, if not in¬ 
variably, be cast out. 

If a piece of 
bone be removed, 
and be immediately 
buried again, in the same animal with aseptic precautions 

the bone dies. 25 Whether it dies immediately after removal, 


u 

Fig. 21.—Stained slide of section of piece of condyle of 
femur buried fresh in the thigh muscles of the animal from 
whom it had just been removed; 922 days after burying. 
The fragment had not decreased greatly in size. Most of 
the bone is alive, some of it is dead. The trabeculae are 
somewhat sparse. 


25 Cowan and Ely: “A Study of Buried Bone,” Journal of Orthopaedic 
Surgery, 1919, i, 100. 

Ely, Leonard W.: “Experimental study of Buried Bone,” Annuls of 
Surgery, 1919, lxx, 747. 






GENERAL CONSIDERATIONS 


51 



Fig. 22.— Stained slide of section of piece of 
head of tibia buried fresh in the thigh muscles 
of the animal from whom it was taken, and 
recovered 473 days later. The fragment had 
decreased decidedly in size, and is well incap- 
sulated. The bone tissue is small in amount, 
the trabeculae are scant, the cortex is thin and 
in places is wanting. Most of the bone is dead, 
but many of the trabeculae show live bone cells, 
especially near their margin—‘border appo¬ 
sition. ’ The marrow is about one-half fibrous 
and one-half fatty. 


Fig. 23.—Photograph of stained slide of sec¬ 
tion of a piece of the condyle buried im¬ 
mediately in the thigh muscles of the animal 
from which it had just been removed, and 
recovered after 374 days. It had decreased 
in size. Most of the bone is dead, but many 
of the trabeculae show life at their edges and 
there are a few trabeculae under the cartilage, 
lying in the midst of dead bone, whose base¬ 
ment substance stains sharply in contrast 
to that of the dead bone, and whose cells 
also stain. 



Fig. 24. —Photograph of a stained slide of a cross section of a fragment of the femoral condyle, 
buried fresh in the thigh muscles of the animal from which it had just been removed, and recov¬ 
ered after 1103 days. The fragment had decreased markedly in size. It was a mere shell and 
cut easily with the knife. Even the shell had been partially replaced by fibrous tissue. The 
bone trabeculae are very few and small—mere fragments—but they are all alive. 



52 


INFLAMMATION IN BONES AND JOINTS 


rn 


Bone-- 


or whether it lives for a short time is not settled, but that 
it can live long enough for the blood vessels which are 
necessary for its nourishment to push their way into it, is 
so improbable, that we are justified in concluding the death 
of the graft to be invariable, until positive proof to the 
contrary shall he adduced. All the experimental evidence 

points in this direction. Those 
who have examined buried 

hone are practically unani¬ 

mous on this point. The evi¬ 
dence on the other side is 

clinical. 

From the moment of im¬ 
bedding of such a piece of 
hone two distinct processes 

arise, one of absorption and 

one of rebuilding, and, accord¬ 
ing to circumstances, one of 
these processes will exceed the 

Fig. 25. —Cross section of piece of condyle other. If the hone have been 

of femur, boiled before being buried in the 

thigh muscles of the animal from which it ,.l 0 enD ficciiPC 

was taken and recovered after 150 days. pidtcU 111 L11C oUl L llooUCo, 

The fragment had decreased greatly in size ■, ., 1 n , • 

and is incapsulated by fibrous tissue. No Where it liaS nO 111110X1011, 

bone cortex is present except for a short . . 

distance. The marrow spaces are bounded althoUffh at all tilUCS CVldeilCeS 
by the connective tissue capsule. The tra- © 

‘thtmT/d^A few of nor bone formation may be 

however show live bone at their margins. ,. w . i 

seen on the edges ot the 
trabecula 1 , it will slowly decrease in size and become 
rarefied, and finally will disappear. It may even last 
for several years, but its fate is always the same. 
On the other hand, if the bone be buried in bone, 
where it will have function, it will persist indefinitely. The 
same processes are set up in this as in the other, but the 
process of repair outweighs that of absorption. Even after 



GENERAL CONSIDERATIONS 


5.'! 

years, areas of dead bone are still visible in it. 20 Nicety of 

«/ 

technique will influence the outcome. The bone must he 
held firmly in contact with the receiving hone, and immov¬ 
able, or it will share the fate of the graft in the soft tissues. 

If boiled bone be employed for the transplant the same 
thing occurs except that its absorption will be more rapid, 
and hence, when employed as a graft between two bones, it is 
not quite so likely to be replaced and rebuilt as is live hone. 
Earth 27 years ago, basing his opinion on experimental 
research, declared that, as all transplanted hone died and 
served only as a scaffold for new bone, the employment of 
live or of boiled bone was a matter of indifference. Clini¬ 
cal experience caused him to modify his opinion, and it has 
caused others to modify theirs. Whether a bone grafted 
in contact with another bone persists, seems to depend upon 
the rapidity with which it is vascularized. 

If a piece of bone with periosteum be examined seven¬ 
teen days after it has been buried alive, its bone and 
marrow are seen to be dead. The marrow is without blood 
vessels. At the periphery, however, where the fragment 
is covered by periosteum, blood vessels are seen pushing 
their way into the bone, and evidences of bone production 
are seen on the edge of the trabeculce . This explains the 
superiority of the living graft to the boiled one; the soft 
tissues at the surface probably live, are quickly vascular¬ 
ized, and thus hasten the vascularization of the graft. 

The above question has a double interest, as bearing 
on the employment of a graft covered with periosteum. 
The periosteum acts not only as soft tissue for vasculariza- 

2C Ely, Leonard W.: “ Ankylosing operations on the Tuberculous Spine; An 
Examination of two Specimens in the Laboratory, “ Journal of the American 
Medical Assn., 1917, lxviii, 183. 

37 Barth: Archiv. fur kHnische Chirurgie, 1893, xlvi, 409:1894, xlviii, 46G. 




54 


INFLAMMATION IN BONES AND JOINTS 


tion, but possibly also as a matrix for the production of 
new bone. 

Albee, who has done much to popularize the use of the 
inlay bone graft and to perfect the technique of its 
insertion, insists that it should be composed of spongy and 



Fig. 26. —Section of condyle of femur of dog, removed at knee-joint resection, and buried 
immediately in his muscle; removed seventeen days later. Photograph of stained slide, 
about ten diameters. The bone and marrow are dead, the bone lacunae are empty. Over the 
inked square the bone is provided with periosteum. Joint cartilage on the right. 

dense bone, and should be covered by periosteum, and that 
like tissue should be applied to like. 

Other rules also should be observed. In old ununited 
fractures the conditions should be made as much like those 
of a fresh fracture as possible. If the ends of the two frag¬ 
ments are sclerosed—eburnated—they must be removed, 




GENERAL CONSIDERATIONS 


55 


and the marrow canals beyond must be opened. Healthy 
hone should be employed for the graft. Its new bed should 
be prepared before it is removed, and after its removal it 
should be inserted as quickly as possible, without unneces¬ 
sary handling, and under strict aseptic precautions. The 
motor saw should be kept cool to prevent killing the graft 



Fig. 27. —This low power photomicrograph, taken of the bone in the inked square in the 
preceding illustration shows well how all activity in bone formation in the dead buried frag¬ 
ment is carried on through the medium of the imbedding tissues. A blood vessel, B, is push¬ 
ing its way from the periosteum into the dead bone, and is starting up the formation of new 
bone. New bone trabeculae, T, T, are forming on the surface of the fragment where it is 
covered by periosteum, and right close to the surface, where blood can reach them, the bone 

cells stain. 

by heat. A motor saw makes the operation much easier, 
but the graft may be removed with hammer and chisel. The 
graft must be fitted accurately in place and must be firmly 
secured there. 

Subsequent immobilization must be furnished hy a 
splint. In old ununited fractures we shall have no assist- 




56 INFLAMMATION IN BONES AND JOINTS 

ance from a splint laid down under the periosteum; hence, 
until enough new bone has been laid down across the gap to 
stand all ordinary strain, external splints must be provided 
to prevent refracture. In fresh grafted fractures, splints 
will be found necessary for a longer time than in simple 
fractures which have not been operated upon, but in old 
ununited fractures the time is much longer, running up to 

three or four months or 
more, and depending upon 
the expected strain. For 
example, after operation for 
ununited fracture of the 
neck of the femur, appara¬ 
tus should he worn for at 
least eight or ten months. 

A piece of the antero¬ 
medial cortex of the tibia, 
less often its crest, or a piece 
of s pht rib, is usually chosen 
for the graft. Sometimes, 
especially with fracture of 
the tibia, a sliding graft is 

used. A small piece of bone 
is removed on one side of the fracture, and a large piece on 

the other. The large piece is then simply slid across the 
gap and the small piece is employed to fill the space left 
at its far end. This procedure obviates the necessity of two 
wounds and is quite feasible, provided that the bone tissue 

of the graft in the vicinity of the fracture is normal 
in structure. 

To avoid the possibility of fracture of the bone from 
which the graft was taken, this bone also must be splinted 
for some time after the operation. Removal of the crest 




Fig. 28.—This shows how the large frag¬ 
ment is slid across into the gap left by the 
removal of the small one, and how the small 
one is used to fill in the gap left proximal to 
the large one. 













GENERAL CONSIDERATIONS 57 

of the tibia weakens the bone much more than does removal 
of a piece of the anteromedial cortex. A twin saw or a 
single saw may be employed. 

In operating on the upper extremity reliable assistants 
can hold the limb after the insertion of the graft. In 
fracture of the femur a special fracture table is almost 
indispensable, so that the splint may he applied without 
disturbing the graft. Success depends largely upon 
attention to details. 

With a fresh fracture one carries the incision down to 
the hone, incises the periosteum longitudinally, strips it 
back enough to permit approximation of the fragments, 
and saws out a gutter in the cortex. In old compound 
fractures the stripping back of the periosteum will occasion 
more difficulty. It is not necessary to remove all the scar 
tissue in these cases, but the ends of the bones must be 
bared, so that the scar tissue no longer lies between them. 
Both marrow canals must be opened, so that the blood 
vessels in each can make their way into the graft. 

Some operators emphasize the importance of stitching 
the periosteum of the graft to that of the receiving hone. 
Others do not find this necessary. 

The great advantage of the dowel in fresh fractures is 
its function as a splint, when it is properly fashioned, but 
its greatest availability is in old fractures of the femoral 
neck. In old fractures of the shafts of hones the inlay graft 
is much to be preferred. 

With an old infected compound fracture it is advisable 
before operating to allow an interval of two or three months 
after all suppuration shall have ceased. With war wounds 
the injection of antitetanic serum should precede 
the operation. 


58 


INFLAMMATION IN BONES AND JOINTS 



Fig. 29.—Low power photomicrograph of stained slide from a tibial graft 
used in an Albee spine operation two years before death from intercurrent 
disease. The graft was united firmly to the vertebral spines. Note the 
different staining reactions of the live and dead bone, the empty lacunae, and 
the blood vessels pushing in from the surrounding soft tissue. 


As far as possible the employment of all non-absorb- 
able substances, such as metal nails, screws, or wire, should 
be avoided. 

Other materials have been employed as substitutes for 
bone in these operations, notably, ivory and the somewhat 




GENERAL CONSIDERATIONS 59 

cheaper walrus tooth.~ s They are not as satisfactory 
as bone. 

Besides its employment in the treatment of fractures, 
the bone graft has many uses, notably in the treatment of 
diseased and flail joints to produce ankylosis, and in the 



Fi g . 30.—Low power photomicrograph of a pseudarthrosis between a bone graft and the 
bone into which it is doweled. The graft is received into a cup-shaped cavity lined by 
fibrous tissue. At the surface of the fibrous tissue is a tissue, provided with villi, not to be 
distinguished from a synovial membrane. The bone of the dowel, as well as that ot the 

receiving cup, is dead. 


Albee operation for tuberculosis of the spine. It has 
been recommended also for a variety of other conditions, 


and enthusiasts predict its wide availability in the future. 

When bone covered with cartilage is buried in the soft 
tissues, the cartilage persists in good condition long after 


28 Koenig, Fritz: “ Ueber die Implantation von Elfenbein zum Ersatz von 
Knochen-und Gelenkenden” Beitraege zur klinischen Chirurgie,” 1913, 


lxxxv, 19. 






60 


INFLAMMATION IN BONES AND JOINTS 


the bone has died. It seems to derive sufficient nourishment 
from the surrounding tissue and does not suffer from being 
cut off from a direct blood supply. Considerable work lias 
been done experimentally in the transplantation of carti¬ 
lage, but no practical results ever have been obtained in 
grafting it where its presence is of real importance, on the 
joint surface of the end of the bone. 

Reports of the transplantation of joints have been 
made.' 1 The results of one case were so good for a while 
that great hopes of the operation were raised, but the hopes 
were not fulfilled, and joint transplantation has given 
place to other measures. 

ANKYLOSIS 

The word ankylosis, or anchylosis, is derived from the 
Greek agkulos, crooked, but the meaning of the term as 
generally employed, is stiffness or loss of motion in the 
joint. As a rule we do not employ it to describe the stiffness 


29 (a) Reiix, Edward: “ Regeneraton des Knochenmarks. . . bei Gel- 

enktransplantation,” von Langenbeck's Archiv., 1921, xcvii, Heft 1.557. 

(b) “ Epiphysentransplantation.” Munchner medicinische Wochenschrift, 
1911, Iviii, 258G. 

Axhausen, G.: “ Ueber den histologischen Vorgang bei der Transplanta¬ 
tion von Gelenkenden.” Archiv. fiir klinische Chirurgie, 1921, xcix. 1. 

Lexer, “ Ueber Gelenktransplantation,” YerhandJungen d. deutsch. 
Oesell. f. Chir., 1910, ii. Medicinische Klinik, 1908, 817. 

Klapp, R.: “Ueber Umpflanzung von Gelenkenden,” Archiv. fiir klinische 
Chirurgie, 1911, xcvi, 386. 

Helferich: “ Zur Frage der Transplantation des Intermediarknorpels,” 
Munchner medicinische IVochenschrift, 1911, lviii. 2796. 

Haas, S. T.: “The Transplantation of the articular end of bone, etc.” 
Surgery Gynecology and Obstetrics, 1916, xxiii, 301. “The Experimental 
transplantation of the epiphysis, etc.” Journal of the American Medical 
Association, 1915, lxv. 1965. 

Heller, E.: “ Versuche ueber die Transplantation der Knorpelfiige.” 
Archiv. fiir Klinische Chirurgie, 1917-18, cix. 1. 





GENERAL CONSIDERATIONS 


61 


present as a physical sign of an active joint inflammation, 
but only that remaining after the inflammation has run its 
course. The subject has received various classifications, of 
which the following is perhaps the best: A true ankylosis 
is - one in which the impairment of mobility is caused by 
change in the joint tissues themselves; in false ankylosis 
it is caused by change in the tissues outside the joints. The 
term contracture is gradually replacing the latter. 

Complete ankylosis means an absence of motion, incom¬ 
plete means a restriction of motion. The former is always 
bony, though a dense fibrous ankylosis may simulate it 
clinically. An incomplete ankylosis may be due to fibrous 
adhesions between the bones, or between one or both of them 
and the capsule, as in the first great type of chronic arthritis, 
or it may be due to a change in the shape of the bone ends 
so that they no longer fit each other, as in the second great 
type of chronic arthritis. 

In order to treat a case of ankylosis intelligently, it is 
advisable for the surgeon to have a fairly clear idea of the 
anatomical changes as well as of their cause, and of all the 
peculiarities of the various joints. No absolute standard 
of treatment has been established, and every case must be 
judged on its merits. We do not get much help here from 
animal experiments. It is almost as hard to produce bony 
ankylosis in a dog’s knee as it is to prevent union of a simple 
fracture of the shaft of one of his bones. 80 

The opinion is general that bony ankylosis follows a 
resection of a joint in man. It often follows resection of the 
knee, if care be taken with subsequent immobilization. I 
think the hip is rather hard to ankylose. Bony ankylosis is 
not to be expected after resection of the ankle or the 

30 Ely, Leonard W.: “Experimental Resection of the Dog’s Knee Joint,” 
dnnala of Surgery, 1919. 




62 INFLAMMATION IN BONES AND JOINTS 

shoulder, and it is notoriously hard to secure in resection of 
the elbow. Exact information is lacking in the toe joints. 



Fig. 31. Bony ankylosis of wrist following an old closed infectious arthritis 

ol unknown etiology. 

but the end of the metatarsal may be cut off in cases of 

hallux valgus with little fear of ankylosis, though some 
stiffness may remain. 




GENERAL CONSIDERATIONS 63 

It is easier to stiffen the joint of the adult than that of 
the child. Normal joints become stiff after immobilization. 
The exact anatomical cause of this stiffness is hard to 
determine. Some say that fibrous adhesions form in the 
joint, and hasten to remove splints in fracture cases and to 
carry out early active and passive motion. Others maintain 
that a normal joint will 
never become perma¬ 
nently ankylosed, no 
matter how long it 
may be immobilized, 
and that the restriction 
of motion is caused by 
contraction of the tis¬ 
sues outside the joint. 

It is hard to say where 
the truth lies. Neither 
side seems to have any 

actual proof. In former Fig. 32.—Old fibrocartilaginous ankylosis of the 

x elbow-joint. One can easily realize the effect of any 

times I held the latter treatment other than operative upon a joint like this. 

view very strongly, but I am not quite so sure as I was. 

As to the treatment of ankylosis, competent authorities 
agree that no attempt should be made to mobilize a joint 
which is the seat of an active inflammation. Motion is the 
worst possible thing for such a joint, and we should assist 
nature in her efforts to provide rest. Pain is nature’s great 
conservative symptom. If a joint is painful, its owner will 
try to keep it at rest. When all evidences of active inflam¬ 
mation are absent, the case is different. 

Two things are important to know in a case of ankylosis. 
The first is its type, whether it is complete or incomplete, 

and whether caused by adhesions between the ends of the 

•/ 

bones, or by their distortion. This is determined by an 



64 


INFLAMMATION IN BONES AND JOINTS 


examination of the joint, and by the Rontgen picture. The 
second thing is the probable cause of the ankylosis. This 
is determined by a careful history, and by the examination 
of the patient himself as well as of his joint. 

Ankylosis from distortion of the bone ends is usually 
caused by the second great type of chronic arthritis, or by 
old joint fractures. Fibrous ankylosis results from tuber¬ 
culous, gonococcic, syphilitic, staphylococcic, streptococcic 
arthritis, and from other forms of arthritis also. Strepto¬ 
cocci and staphylococci may also cause a bony ankylosis. 
Syphilis probably never does. Simple intraarticular fract¬ 
ures may result in bony ankylosis probably through the 
building of a bony bridge in the capsule. A rare form of 
bony ankylosis has been described in the elbow, following* 
a slight injury, without any evidence of fracture. It 
seems to have been essentially an ossification of the capsule. 
I have seen it follow an unreduced dislocation of the hip in 
an elderly man. 

According to Ollier ' 1 and Mauclaire, 2 after a bony 
ankylosis, the structure of the bone at the site of the former 
joint changes. The diameter slowly lessens, the spongy 
bone is absorbed, the cortical bone thickens, the proximal 
and distal medullary canals extend until sometimes they 
join, the lymphoid marrow gives place to fatty mar¬ 
row, and finally a typical section of a shaft of a long 
hone may be established. I have never had the oppor¬ 
tunity to examine a specimen in the laboratory, but I have 
watched with the Rontgen rays the changes in the archi¬ 
tecture for as long as ten years after knee joint resections. 

31 Ollier: “Diet.” encycl. des sciences Medicales, Paris, 1870, Ankvlose 

p. 191. J ^ ’ 

!2 Mauclaire: “ Noveau Traite de Chirurgie,” Paris, 1909. Ankvloses 
p. 235, ' * 



Fig. 33.—Tuberculous knee ten years after resection. 


GENERAL CONSIDERATIONS 


o5 



o 




66 


INFLAMMATION IN BONES AND JOINTS 


and have seen the bone remodelled along these lines, but 
apparently not completely canalized. Complete canaliza¬ 
tion takes a long time. Spongy bone has been observed 



Fig. 34. —Ankylosis caused by new bone in the joint capsule. Mo¬ 
tion was restored in this case by the removal of the bone, and the 
insertion of a fascial flap over its base. 

two and a half years after the resection of a tubercu¬ 
lous knee . 33 

The treatment of ankylosis naturally falls under 
the head of that of the diseases which cause it, but certain 
aspects of it may be considered here. 


33 Wagstaff, Mr.: Path. Soc. Trans., 1868-69, xx, 264: 



GENERAL CONSIDERATIONS 


67 


If there be reason to believe that tuberculosis was the 
cause, most authorities advise that the ankylosis be left 
absolutely alone. Even many years after all active symp¬ 
toms have subsided, foci of infectious material may remain 
locked up in the bone marrow, or in the fibrous adhesions 
of the joint, capable, if they be set free, of lighting up the 
disease afresh. 

The ankylosis following joint fracture may sometimes 
be improved by remodelling the bone ends by operation. 
Each case must he judged on its merits. Sometimes what 
appears to be a firm ankylosis turns out to be a plate of 
bone in the capsule continuous with one of the articulating 
hones. If it be removed, and a flap of fat or of fascia be 
swung over its base, free motion may be restored. In 
dealing with the knee joint it is well to find out if the tibio¬ 
femoral articulation, or the femoro-patellar, or both joints 
together, are involved. 

When the ankylosis is caused by fibrous adhesions, these 
may be broken up forcibly under an anaesthetic (brisement 
force), and then the joint may be immobilized in a dif¬ 
ferent attitude. It may be necessary to repeat the 
manoeuvre several times. In point of fact not much can 
be expected of this method. 

Physical therapy—baking, massage, hydrotherapy, 
gentle active and passive motion, etc.—at present has quite 
a vogue. Fibrolvsin is more or less of a medical relic. 4 

ARTHROPLASTY 

The modern attempts at forming a new joint are 
usually dated from Ollier. Helferich followed Ollier. In 
this country the operation was first strongly advocated by 
Murphy. The subject has been investigated and de- 

34 Sidorenko, P.: “ Experimentelle und klinische Untersuchungen ueber die 
Wirkung des Fibrolysins etc.” Dent. Z. f. Chir., 1911, cx, 89: 




68 


INFLAMMATION IN BONES AND JOINTS 


veloped by Payr, Sumita, Allison and Brooks, Baer and 
many others. 

The simplest form of the operation of arthroplasty is 
the division of ankylosing tissue, possibly supplemented by 
a shaping of the bones. Little is to be expected from this. 
Its poor results gave rise to attempts to supplement it with 
the interposition of various substances, organic and inor¬ 
ganic. Ollier turned in periosteum between the two bones. 
Others interposed muscle flaps, fat and fascia flaps, animal 
membranes of various kinds, and even inorganic sub¬ 
stances. The flap of fat and fascia is the one now 
most employed. 

Most writers affirm that temporomaxillary arthroplasty 
gives the best results. Perhaps this is because the operator 
on this articulation has but one object, to mobilize it. In 
other joints the fear of instability enters into the calcula¬ 
tion. An unstable knee, for instance, is much worse than 
a stiff one, though many knees have been mobilized without 
losing their stability. The hip offers a better prognosis 
than the knee. 

The Operation. —Artificial ischaemia is not advisable, 
though Murphy employed it. The joint is opened so as to 
provide free access to it. In the case of a fibrous anky¬ 
losis, all the fibrous adhesions are dissected away, and also 
the contracted and cicatricial capsule. This is important. 
In a bony ankylosis the bone is divided at the site of the 
former joint, and the bone ends are trimmed to a shape as 
near their former shape as possible. Plenty of the bone 
must be removed. In old fibrous ankylosis also, the bones 
should usually be reshaped. All bleeding must be checked. 
The tissue to be interposed is then sutured carefully over 
one articulating surface. If an attached flap is used, it is 
jiartially dissected from its bed in the neighborhood, and 



GENERAL CONSIDERATIONS 69 


swung between the bones to be sutured. The wound 
is closed. 

The period of the subsequent immobilization is a ques¬ 
tion of circumstances, and largely of opinion. It is possible 
to err on either side. Obviously motion should begin as 
soon as practicable, but not soon enough to disturb the 
healing of the wound. Payr begins motion in about one 
week, using traction after the first forty-eight hours. Baer 
puts his cases up in plaster of Paris for about four weeks. 
I incline to an average of ten days to two weeks. Active 
as well as passive motion should be carried out. Electrical 
stimulation and massage of the atrophic muscles may begin 
almost immediately. Small ham atom at a should be 
aspirated. The patient’s cooperation is almost a sine qua 
non, and patience and interest on the part of the oper¬ 
ator also. 

In knee operations long medial and lateral incisions 
are the favorite. A separate long incision from near the 
proximal end of the lateral incision lays bare the fascia 
almost up to the trochanter. A strip of this about 10 cm. 
wide and 20 cm. long is then incised on its proximal, 
anterior and posterior margins, dissected clear of the 
vastus lateralis with care, and still attached at its distal 
border, is drawn through a tunnel made between this inci¬ 
sion and the first lateral one. It is sutured carefully over 
the entire end of the femur, so that it lies between the femur 
and the tibia, and between the femur and the patella as 
well. Before the wound is closed all bleeding must 
be stilled. 


Corner’s long anterior incision 85 with splitting of the 


35 Corner, E. M.: “The Surgery of the Knee.” Journal of the American 
Medical Association, 1914, lxiii, 1069. 




70 


INFLAMMATION IN BONES AND JOINTS 


patella, should be admirably adajDted to this operation. 
(Fig. 96.) Kirschner’s 36 has also been recommended. 

In many cases of knee ankylosis, the tibio-femoral 
joint is normal and the entire trouble resides between the 
femur and the patella. The flap then would be interposed 
solely between these two. 

In hip joint operations Baer favors the anterior in¬ 
cision, running clistally from the anterior superior spine, 
about 15 cm. long between the tensor fascia? lata? and the 
sartorius. Sprengel’s incision 37 or Smith-Peterson’s slight 
modification of it, 38 which add to the anterior incision one 
running from the anterior superior spine along the ilium 
just distal to the crest, gives a better exposure. (Fig. 91.) 
Murphy favors a large lateral U-shaped incision five inches 
wide with its base proximal and its convexity distal. (Fig. 
92.) The trochanter occupies the centre of the flap. The 
flap includes the skin, fat and fascia lata and is reflected 
proximally. A threaded curved needle, passed around the 
trochanter draws a Gigli saw after it, and the trochanter 
is then divided and drawn proximally. This gives an excel¬ 
lent exposure of the joint. A flap of fat and fascia is dis¬ 
sected from the large original flap. 

In the elbow, medial and lateral incisions may be em- 

%/ 

ployed or a long posterior one with transverse sawing of 
the olecranon and its subsequent wiring or suturing. 

In the shoulder, the ordinary anterior incision will be 
found useful, between the deltoid and pectoralis major, or 
the posterior incision of Ivocher. 39 

36 Kirschner: “ Ein neues Operationsverfahren zur schonenden Eroeffnung 
des Kniegelenks.” Beitr. z. klin. Chir., 1910-1911, lxxi, 703. 

Sprestgee: Zur operativen Nachbehandlung alter Huftresectionen,” 

Archiv. f. klin. Chir., 1898, lvii, 837: 

Smu h-Peterson, M.N.: A new supra-articular, sub-periosteal approach 
to the hip-joint.” American Journal of Orthopaedic Surgery, 1917, xv. 592. 

3I> Kocher, Theodor: “ Mittheilungen aus der chirurgischen Klinik in 
Bern.” Arch. f. klin. Chir., 1888, xxxvii, 777. 




GENERAL CONSIDERATIONS 


71 


In temporomaxillary arthroplasty, Murphy 40 advo¬ 
cated an L-shaped incision, the perpendicular arm about 
4 cm. long running immediately in front of the ear, from 
the zygoma, and the horizontal about 2 cm. long, along the 
upper border of the zygoma. He removed about 1 cm. 
from the head and neck of the bone, and employed a fascial 
flap from the temporal muscle. 

BIBLIOGRAPHY 

BONE GRAFTING 

Albee, Fred H.: “Bone-graft surgery.” Phila. and London, W. B. Saunders 
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Albee, Fred H.: “An experimental study of bone growth and the spinal bone 
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Albee, Fred H.: “The fundamental principles involved in the use of the bone 
graft in surgery.” Am. Jour. Med. Sci., 1915, cxlix, 313. 

Axhausen, Georg: “ Arbeiten aus dem Gebiet der Knochenpathologie und 
Knochenchirurgie.” Arch. f. klin. Chir., 1910-11, xciv, 241. 

Axhausen, Georg: “Die histologischen und klinischen Gesetze der freien 
Osteoplastic.” Arch. f. klin. Chir., 1908-09, lxxxviii, 23. 

Axhausen, Georg: “ Histologische Untersuchungen iiber Knochentransplan- 
tation am Menschen.” Deutsche Ztschr. f. Chir., 1907-08, xci, 388. 
Axhausen, Georg: “ Ueber den Vergang partieller Sequestrirung transplan- 
tirten Knochengewebes.” Arch. f. klin. Chir., 1909, Ixxxix, 281. 

Axhausen, Georg: “Ueber plastische Operationen am Knochensystem.” Fort- 
chr. d. Med., 1909, xxvii, 369. 

Bancroft, Frederic W.: 44 The use of small bone transplants in bridging 
a bone defect.” Ann. Surg., 1918, lxvii, 457. 

Barth: “ Knochenimplantation.” Beitr. z. path. Anat., 1895, xvii, 65. 

Barth: “Ueber Osteoplastik.” Arch. f. klin. Chir., 1908, lxxxvi, 859. 
Baschkirzen, N. J., and Petron, N. N.: 44 Beitriige zur freien Knochenuber- 
pflanzung.” Deutsche Ztschr. f. Chir., 1912, cxiii, 490. 

Bergeman, W.: “Wie lange nach dem Tode oder nach der Amputation 
bleibt der Knochen transplantationsfaehig.” Arch. f. klin. Chir., 1909, 
cx, 279. 

Berger, Hermann, und Schwab, M.: “Knochen und Gelenktransplantation- 
en.” Deutsche med. Wchnschr., 1912, xxxviii, 2029. 

Bier, August: “ Beobachtungen iiber Knochenregeneration.” Arch. f. klin. 

Chir., 1912-13, c, 91. 

Bittner, Wilhelm: “ Ueber Knochenplastik nach Resektion an langen Rohren- 

knochen.” Zentrlbl. f. Chir., 1910, xxxvii, 571. _ 

40 Murphy. John B.: Journal of the American Medical Association. 1914, 
lxii, 1785. 





72 


INFLAMMATION IN BONES AND JOINTS 

§ 

Brooks, Barney: “Studies in bone regeneration.” Ann. Surg., 1917, lxvi, 625. 

Brooks, Barney: “Studies in bone transplantation; A study of a method 
of increasing the osteogenetic power of a free bone transplant.” Ann. 
Surg., 1919, lxix, 113. 

Brooks, Barney: “Studies in regeneration and growth of bone.” Ann. Surg 
1917, lxv, 704. 

Brooks, Barney: “Studies in bone transplantations, etc.” Archives of Surg., 
1920, i, 284. 

Codman, Ernest A.: “Bone transference.” Ann. Surg., 1909, xlix, 820. 

Davis, John S.: “A comparison of the permanence of free transplants of 
bone and cartilage.” Ann. Surg., 1917, lxv, 170. 

Davis, John S.: “Partial epiphysial transplantation for defect in fibula.” 
Ann. Surg., 191G, lxiv, 519. 

Davis, John S. and Hunnicutt, John A.: “The osteogenic power of 
periosteum.” Johns Hopk. Hosp. Bull., 1915, xxvi, 69. 

Enderlen: “Zur Reimplantation des resecirten Intermediarknorpels beirn 
Kaninchen.” Deutsch Ztschr. f. Chir., 1899, li, 574. 

Gallie, W. E.: “The history of a bone graft.” Am. Jour. Orth. Surg., 1914, 
xii, 201. 

Gallie, W. E., and Robertson, D. E.: “Repair of bone.” Brit. Jour. Surg. 
1919, vii, 211. 

Gallie, W. E.: “The transplantation of bone.” J. A. M. A., 1918, Ixx, 1134. 

Groves, Ernest W. Hey: “Methods and results of transplantation of bone 
in the repair of defects caused by injury or disease.” Brit. Jour Surg 
1917-18, v, 185. 

Haas, S. L.: The experimental transplantation of the epiphysis.” J. A 3/ A 
1915, lxv, 1965. 

Haas, S. L.: Free transplantation of bone into the phalanges.” J, A. M. A 
1914, lxii, 1147. 

IIelferich : “ Versuche fiber die Transplantation des Intermediarknorpels 
wachsender Rohrenknochen.” Deutsche Ztschr. f. Chir., 1899, li, 564. 

Henderson, M. S.: 4 he use of beef-bone screws in fractures and bone 

transplantation.” J. A. M. A., 1920, lxxiv, 715. 

Hoglund, Emil J.: New method of applying autogenous intramedullary bone 
’transplants.” Surgery, Gyn. Obst., 1917 , xxiv, 243 . 

Jost, Otto: “ Beitriige zur Osteoplastik an den Extremitaten.” Beitr. z. 
klin. Chir., 1914-15, xcv, 86. 

Kauscii, W.: “Zur Frage der freien Transplantation toten Knochens.” 
Zentrlbl. f. Chir., 1909, xxxvi, 1379. 

Konig F.: “ Erfolgreiche Gelenkplastik am Ellbogen durch Implantation einer 
Elfenbeinprothese.” Munch, med. Wchnschr., 1913, lx, 1136. 

Konig, F.: “ Ueber die Implantation von Knochen und Gelenkenden.” Beitr. 
z. klin. Chir., 1913, lxxxv, 91. 

Klapp, R. : “Fall von ausgedehnter Knochentransplantation.” Deutsche 
Ztschr. f. Chir., 1900, liv, 576. 


GENERAL CONSIDERATIONS 


73 


Lawen: “ Zur Histologie des frei transplantirten periostgedekten Knochens 
beim Menschen.” Arch. f. klin. Chir., 1909, xc, 469. 

Lexer, Erich: “Die praktische Verwendung der freien Transplantation.” 

Miinch. med. Wchnschr., 1913, lx, 2059. 

Lexer, Erich: “ Ueber Gelenktransplantation.” Arch. f. klin. Chir., 1909, 
xc, 263. 

Mac Ausland, W. R., and Wood, B. E.: “Transplantation of the fibula." 
Surg. Gynec. Obst., 1912, xiv, 380. 

McWilliams, Clarence A.: “ Bone transplantation.”^ nn. Surg., 1916, lxiii, 185. 
McWilliams, Clarence A.: “Transplantation of bone.” Med. Record, 1916, 

xc, 498. 

Murphy, John B.: “ Contributions to the surgery of bones, joints and tendons.” 
J. A. M. A., 1912, lviii, 985, 1094. 

Murphy, John B.: “Osteoplasty.” Surg., Gynec. Obst., 1913, xvi, 493. 
Noesske, K.: “ Ueber den plastischen Ersatz von ganz oder teilweise verlorenen 
Fingern. . .” Miinch. med. Wchnschr., 1909, lvi, 1403. 

Petrow, N. N.: “ Zur Frage nach der Quelle der Regeneration bei Knochen- 
iiberpflanzung.” Arch. f. klin. Chir., 1914, cv, 915. 

Phemister, D. B. : “ The fate of transplanted bone and regenerative power of 
its various constituents.” Surg., Gynec. Obst., 1914, xix, 303. 

Phemister, D. B.: “Necrotic bone and the subsequent changes which it under¬ 
goes.” J. A. M. A., 1915, lxiv, 211. 

Rehn, Eduard: “Zur Regeneration des Knochenmarks bei der homoplastichen 
Gelenktransplantation im Thierexperiment.” Arch. f. klin. Chir., 1912, 
xcvii, 35. 

Schewandin: “ Endresultate der Lexer’schn Arthrodese am Sprunggelenk.” 
Arch. f. klin. Chir., 1913, ci, 1009. 

Stieda, A.: “Beitrage zur freien Knochenplastic.” Arch. f. klin. Chir., 1911, 
lciv, 831. 

Stuckey, L.: “Ueber die freie Knochentransplantation bei der Pseudarth- 
rosenbehandlung.” Beitr. z. klin. Chir., 1912, lxxx, 83. 

Todyo, Tsuneharu: “The growth of free bone transplants.” Surgery, Gyn. 
Obst., 1917, xxiv, 701. 


ARTHROPLASTY 

Ollier, L. X. E. L.: “ Traite experimental et clinique de la regeneration des 
os.” Paris, 1867, Masson. 

Helferich: “ Ein neues Operationsverfahren zur Heilung der knoechernen 
Kiefergelenksankylose.” Arch. f. klin. Chir., 1894, xlviii, 864. 

Helferich: “Ueber operative Nearthrosis.” Miinch. med. Wchnschr., 1913, 
lx, 2769. 

Murphy, John B.: “Ankylosis. . . Arthroplasty, clinical and experimental.” 
J. A. M. A., 1905, xliv, 1573. 

Murphy, John B.: “Arthroplasty.” Ann. Surg., 1913, lvii, 593. 

Murphy, John B.: “Arthroplasty for intra-articular bony and fibrous anky¬ 
losis of temporomaxillary articulation.” J. A. M. A., 1914, lxii, 1783. 


74 


INFLAMMATION IN BONES AND JOINTS 


Payb, E.: “ Ueber die operative Behandlung von Kniegelenksankylosen.” 
Arch. f. klin. Chir., 1912, xcix, G81. 

Payr, E.: “ Ueber die operative Mobilisierung ankylosierter Gelenke.” 

Munch, med. Wchnschr ., 1910, lvii, 1921. 

Payr, E.: “ Weiter Erfahrungen ueber die operativer Mobilisierung anky¬ 
losierter Gelenke. . .” Deutsche Ztschr. f. Chir., 1914, cxxix, 341. 

Payb: “Ueber die blutige Gelenkmobilisierung. . Wien. m. Wnsch., 1915, 
lxv, 1102. 

Sumita, Masao: “ Experimentelle Beitrage zur operativen Mobilisierung 
ankylosierter Gelenke.” Arch. f. klin. Chir., 1912, xcix, 755. 

Allison, Nathaniel, and Brooks, Barney: “Ankylosis.- an experimental 
study.” Surg. Gynec. Obst., 1914, xix, 568. 

Allison, Nathaniel, and Brooks, Barney: “Arthroplasty: experimental 
and clinical methods.” Am. Jour. Orth. Surg., 1918, xvi, 83. 

Allison, Nathaniel, and Brooks, Barney: “The mobilization of ankylosed 
joints: an experimental study.” Surg., Gynec. Obst., 1913, xvii, 645. 

Baer, William S.: “Arthroplasty with the aid of animal membrane.” Am. 
Jour. Orth. Surg., 1918, xvi, 1, 94, 171. 

Baer, William S.: “A preliminary report of the use of animal membrane 
in producing mobility in ankylosed joints.” Am. Jour. Orth. Surg., 1909- 
1910, vii, I. 

Axhausen, G.: “Ueber den histologischen Vorgang bei der Transplantation 
von Gelenkenden, insbesondere iiber die Transplantationsfahigkeit von 
Gelenkknorpel und Epiphysenknorpel.” Arch. f. klin. Chir., 1912, xcix, 1. 

Blair, V. P.: “ Operative treatment of ankylosis of the mandible.” Surg. 
Gynec. Obst., 1914, xix, 436. 

Cramer, F.: “Ueber die Losung der verwachsenen Kniescheibe.” Arch. f. 
klin. Chir., 1901, lxiv, 696. 

Ely, Leonard W., and Cowan, John Francis: “Experimental resection of 
the dog’s knee joint; Bone and joint studies, 1.” Stanford University, 
California. Published by the University. 1916. 

Ely, Leonard W.: “Experimental resection of the dog’s knee joint.” Ann. 
Surg., 1919, lxx, 586. 

Henderson, M. S.: “What are the real results of arthroplasty.” Am. Jour. 
Orth. Surg., 1918, xvi, 30. 

Hoffa, A.: “Die Mobilisierung knochern verwachsener Gelenke.” Ztschr. 
f. Orth. Chir., 1906, xvii, 1. 

Hoffmann, H.: “Ueber Kieferegelenksankylose mit ‘ Vogelgesicht’ Bildung.” 
Beitr. z. klin. Chir., 1914, xcii, 92. 

Hofmann, M.: “ Weitere Untersuchungen und Erfahrungen iiber Periost- 
transplantation bei Behandlung knocherner Gelenkankylosen.” Beitr. z. 
klin. Chir., 1908, lix, 717. 

Hohmeier, F., and Magnus, G.: “Zur Frage der Weichteilimplantation bei 
Gelenkresectionen.” Beitr. z. klin. Chir., 1914, xciv, 547. 

Klapp: “Ueber Umpflanzung von Gelenkenden.” Arch. f. klin. Chir., 1912, 
xcvi, 386. 


GENERAL CONSIDERATIONS 75 

Kirschner, Martin: “ Ein neues Operationsverfahren zur schonenden 
Eroffnung des Kniegelenkes.” Beitr. z. kiln. Chir., 1910-11, lxxi, 703. 

Konig, F.: “ Erfolgreiche Gelenkplastik am Ellenbogen durch Implantation 
einer Elfenbeinprothese.” Miinch. med. Wchnschr., 1915, lx, 1136. 

Kuttner, Hermann: “Die Transplantation aus der Leiche.” Beitr. z. klin. 
Chir., 1911, lxxv, 1. 

Lexer, Erich: “ Ueber freie Transplantationen.” Arch. f. klin. Chir., 1911, 
xcv, 827. 

Lexer, Erich: “Ueber Gelenktransplantation.” Arch. f. klin. Chir., 1909, 
xc, 263. 

MacAusland, W. R.: “Ankylosis of the elbow.” J. A. M. A., 1915, lxiv, 312. 

Neff, James M.: “Arthroplasty.” Sure/, Gynec. Obst., 1912, xv, 529. 

Phemister, D. B., and Miller, E. M.: “The method of new joint formation 
in arthroplasty.” Surg., Gynec. Obst., 1918, xxvi, 406. 

Rehn, Eduard: “Die Fetttransplantation.” Arch. f. klin, Chir., 1912, 
xcviii, 1. 

Reiner, Hans: “Ueber die funktionellen Resultate der Resektion des 
Ellbogengelenks. . .” Deutsche Ztschr. f. Chir., 1910, civ, 209. 

Schmerz, H.: “Ueber operative Kniegelenksmobilisierung und Function- 
serstellung durch Amnioninterposition.” Beitr. z. klin. Chir. 1911, lxxvi, 

261 . 

Segale, Carlo: “ Experimentelle Untersuchungen liber die Regeneration 
der Kniegelenkkapgel nach Totalexstirpation.” Beitr. z. klin. Chir., 1913, 
lxxxvii, 299. 

Segale, Carlo: “Ueber die Regeneration der Synovialmembran und der 
Gelenkkapsel.” Beitr. z. klin. Chir., 1913, lxxxvii, 259. 











SECTION II. 

ACUTE OSTEOMYELITIS AND ARTHRITIS 




CHAPTER I 


ACUTE SUPPURATIVE HiEMATOGENOUS 

OSTEOMYELITIS 

Of the four usual causes of inflammation, mechanical, 
thermal, chemical, and bacterial, the last two only are of 
great importance in inflammations of the bone marrow. 
Its situation protects it from ordinary degrees of heat and 
cold, and also from all injuries except fracture. 1 After a 
simple fracture the changes in the marrow are essentially 
those incidental to the repair of the bone. 

Injury seems to do little permanent damage to the 
marrow. If the marrow be curetted from the shaft of a 
laboratory animal it quickly regenerates, and, after a com¬ 
paratively short time shows no trace of the injury. 2 It is 
important to remember this fact, on account of the per¬ 
sistent tendency to ascribe to trauma a leading role in most 
diseases, acute and chronic, of bone as well as of other tis¬ 
sues. As our knowledge becomes more exact, trauma 
usually sinks more and more into the background. 

As to the influence of chemical agents, the evidence for 
one, such as phosphorus, is positive, that for others, such as 
toxines, is largely presumptive. 

The cause of osteomyelitis in an overwhelming propor¬ 
tion of cases is infection, and the chief bacterial infectious 
agents are the staphylococcus and streptococcus pyogenes, 
the tubercle bacillus, the bacterium coli commune, the 
gonococcus, the treponema pallidum, the diplococcus, the 
typhoid bacillus, and the pneumococcus. 

1 Extreme low temperature may, of course, cause necrosis of the marrow. 

2 Ely, Leonard W.: “Regeneration of the bone marrow. Bone and Joint 
Studies I.” Stanford University 1916, Published by the University. 


79 




80 


INFLAMMATION IN BONES AND JOINTS 


It is customary to divide cases of osteomyelitis into 
acute and chronic, and this division, while by no means 
exact, is convenient and will be adojffed here. Some cases 
are acute from the start, run a typical course, and end in 
recovery or in death. Others are essentially chronic. Still 
others start with all the earmarks of an acute disease, and 
then settle down into a chronic stage, to last indefinitely, or 
possibly to recover under appropriate treatment. Again, 
what has been from the beginning a chronic disease may at 
any time take on all the appearance of an acute one. 

ACUTE OSTEOMYELITIS 

The one great cause of acute osteomyelitis is infection. 
The infection may be carried in from the outside, as with 
compound fractures; it may make its way into the bone 
from neighboring tissues, as with acute arthritis or deep 
suppurations; or it may be blood borne. The last consti¬ 
tutes a special disease of itself, with a well defined clinical 
picture, and will be considered first. 

What is commonly known as osteomyelitis, or acute 
osteomyelitis, is a suppurative inflammation of the bone 
marrow, occurring almost always in children or in ado¬ 
lescents, with an acute onset, febrile course, and marked 
constitutional reaction, and ending in the death of a greater 
or less amount of marrow and of bone. Its cause is usually 
the staphylococcus pyogenes aureus, less often the staphy¬ 
lococcus pyogenes albus or the streptococcus pyogenes, and 
rarely the bacterium coli commune. The organism may 
exist alone, or the infection may be a mixed one. With 
invasion by streptococci a marked tendency to involve¬ 
ment of the neighboring joint has been noted. In many 
instances the organism can be cultivated from the blood. 

Occasionally the offending organism is brought from 


HEMATOGENOUS OSTEOMYELITIS 


81 


some known suppurating focus somewhere else in the 
body, usually its place of origin is not known. Its favorite 
port of entry has been assumed to be an abrasion of the 
skin, however small, and the fact that the staphylococcus 
albus is the most common infecting agent lends color to this 
assumption. The tonsil has been under suspicion, not only 
on account of the occasional sequence of the disease on 
scarlet fever, but also because of the causal relation of the 
tonsil to acute and to chronic arthritis. 

The importance of trauma as a contributing cause has 
been much debated. The results of animal experiments 
are contradictory. Clinical opinion can be found on both 
sides of the subject. At present we must consider the 
question as not proved. 

The sequence of the disease upon an infectious disease, 
especially upon scarlet fever, has been noted, and also its 
sequence upon chilling of the surface. 

As has been said, acute osteomyelitis is essentially a 
disease of childhood and adolescence. It is most frequent 
in the second decade of life, and many cases occur in the 
first and third decades. Lexer taught that its location in 
the bones was dependent upon the arrangement of the 
blood-vessels about the epiphysial line. Klemm 3 considers 
acute osteomyelitis as simply a suppurative inflammation of 
lymphoid tissue, similar to that of lymphoid tissue any¬ 
where else in the body, and only modified and aggravated 
by the rigid bony shell in which it runs its course. I ad¬ 
vanced this reason for the occurrence of marrow tubercu¬ 
losis ten years ago. 4 

Acute osteomyelitis almost invariably begins in the 

3 Klemm, Paul: “Die Osteomyelitis des Kindesalters,” Berlin, Verlag 

von S. Karger, 1914. 

4 Ely, Leonard W.: “Joint Tuberculosis,” William Wood and Company, 

1911. 

6 



8 2 


INFLAMMATION IN BONES AND JOINTS 


metaphysis 5 of one of the long bones, especially in that of 
the femur and of the tibia, less often in that of the humerus. 
The purulent inflammation spreads in the spongy bone, 
killing the marrow and the bone as it goes, and the process 
then adopts one of four different courses. 

1. The Typical Severe Spreading Osteomyelitis. 
—The inflammation travels widely in the spongy bone in 
the general direction of the central marrow canal, gains 
this, and involves its,marrow for a greater or smaller dis¬ 
tance, sometimes reaching the epiphysial line at the other 
end of the bone. It also passes through the minute canals 
in the cortex, and comes to the under surface of the peri¬ 
osteum. It runs along between the cortex and the 
periosteum, dissecting them apart. If an operation has 
not been undertaken by this time, or death has not inter¬ 
vened, the pus breaks through the periosteum, burrows in 
every direction, and finally makes its way to the surface. 
We have then the necrotic shaft—the sequestrum—filled 
with pus, and lying within the periosteum, bathed in pus, 
and connected with the surface by sinuses. 

Death, from sepsis, from ulcerative endocarditis, or 
from metastases in the kidneys or in other organs, would 
probably have closed the scene; if not, then with the free 
discharge of pus, the disease settles down to the chronic 
stage. In areas the periosteum may become adherent to 
the necrotic bone beneath it. After a few weeks, bone 
formation begins in or under the periosteum, and proceeds 
until the necrotic shaft is enclosed in a more or less com¬ 
plete shell of bone (the involucrum) perforated by holes 
for the discharge of pus—cloacae, sewers. 

A stage is thus reached which, without outside aid, will 
last indefinitely. The dead shaft, locked up in its rigid 

5 The metaphysis is that portion of the spongy bone which lies shaftward 
from the epiphysial line. 








HEMATOGENOUS OSTEOMYELITIS 


83 


case, is incapable of absorption, and remains permanently 
as a foreign body. In the end the patient may die from 
the effects of the prolonged suppuration. 

Not always does the disease reach the extreme limits 
detailed above. It may be halted at any point by nature’s 
protective reaction in the marrow, usually by a fibrosis. 
The wall of defence may slowly be reinforced by bone, and 
this, with the periosteal bone, forms a perforated box, in 
which lies the cylinder of sequestrated shaft, more or less 
continuous with it in structure. 

2. The Superficial Form. —In this the disease, 
starting as in the preceding form, near the epiphysial disc, 
and probably near the cortex, never reaches the central 
marrowcanal,but breaking through the thin cortex near the 
end of the bone, gains the under surface of the periosteum, 
and spreads shaftwards beneath it. It kills the superficial 
part of the cortex, and filling the space between it and the 
periosteum with pus, lifts the periosteum off, perforates 
it, and then, burrowing through the soft tissues, makes its 
way to the surface. This form of the disease is wont to be 
less severe than the preceding. 

3. The Circumscribed Form. —Brodie’s abscess. 0 In 
this form the disease remains localized in the metaphysis. 
An abscess forms, usually not of great diameter, and 
becomes walled off by dense bone. It may remain indefi¬ 
nitely stationary, or, according to some writers, may break 
out later, and spread through the bone, like the other 
forms. During its existence it may give rise at any time to 
a sterile effusion in the joint, as may the other three forms. 
It is said to be one of the causes of the so-called inter¬ 
mittent synovitis, or hydroarthrosis. Presumably Brodie’s 
abscess is caused by bacteria of a low degree of virulence. 

6 See an interesting article by Walter M. Brickner: “Chronic medullary 
abscess in the long bones,” Annals of Surg., 1917, lxv, 483. 





84 


INFLAMMATION IN BONES AND JOINTS 


4. The Articular Form. —Starting at or near the 
same place as the three preceding, the disease shows a 
marked tendency to spread towards the joint, perhaps 
spreading shaftward also. It may perforate the epiphy¬ 
sial cartilage, and involve the epiphysis, and then, having 
killed the joint cartilage, in whole or in part, break into the 
joint and become an arthritis. This is the “ acute epiphy¬ 
sitis ” of some writers. The epiphysis may be separated by 
the inflammation beneath it. The disease may break 
directly into the joint without perforating the epiphysial 
cartilage. In either case, the result is the same. Accord¬ 
ing to most writers, this type of case is usually caused 
by the streptococcus, less often by the pneumococcus or the 
typhoid bacillus. 

It is seen therefore that all four forms of the disease 
are the same in their pathological characteristics. They 
differ only in their details. Their course may be checked, 
modified, or changed by operative interference. 

Osteomyelitis (periostitis) albuminosa (serosa) 
is a rather rare form of the disease, usually occurring 
in the femur, with an acute and severe onset, and then 
a milder and chronic course which may last for several 
months. Suppuration does not result, but sequestra form, 
and when at length the fluctuating swelling is opened, the 
fluid is found to be thin, serous, synovia-like. The disease 
is caused by the same organisms as the other forms. 

Symptomatology. —Acute osteomyelitis usually be¬ 
gins suddenly with the customary symptoms of an acute 
infection, chill, high fever, rapid pulse, etc. Sometimes the 
onset is preceded for a few days by headache, malaise, and 
pain in the limbs. The patient complains of severe pain in 
the vicinity of a joint, most often the knee, but not in the 
joint itself. Motion of the joint is usually not very pain- 



HEMATOGENOUS OSTEOMYELITIS 


85 


ful, but pain is caused by prolonged pressure over the af¬ 
fected region, or by percussion. Redness and swelling, 
often oedematous, soon appear, and the oedema may con¬ 
tinue distal to the seat of trouble. As soon as the process 
breaks through the cortex, a fluctuating swelling appears. 
The neighboring joint sometimes fills with fluid, which in 
the majority of cases is sterile. The leucocyte count is 
very high, and cultures of the offending organisms may 
often be made from the blood. The subcutaneous veins 
are prominent, the adjacent lymph nodes are enlarged. 

The patient rapidly becomes worse, and often sinks 
into the so-called typhoid state, with coated tongue, 
delirium, etc. The fever as a rule is continuous. A fluctu¬ 
ating temperature is a sign of metastases. The urine is 
concentrated, and often contains albumin. Cutaneous 
eruptions may be present. 

Such a picture is comparatively easy to recognize. On 
the other hand, swelling may be absent, as may all local 
physical signs of disease, and the delirium and coma may 
be so early and so profound that the patient is not in a 
position to complain of pain. If the disease breaks into 
the joint, the evidences of an acute arthritis are added. 

The diagnosis in most cases is easy. The acute onset, 
with high fever, usually with a chill, the painful swelling in 
the neighborhood of a joint, extremely sensitive to pres¬ 
sure, with dilated superficial veins, and local oedema, 
present a characteristic picture. When the disease is in the 
region of the hip, buried deeply in the muscles, its recogni¬ 
tion is not so simple. The appearance of the fluctuating 
swelling removes all doubt. 

The X-rays give us, as a rule, little help during the first 
week. After that, changes in the bone are evident. These 
show in the increased permeability of the bone to the rays, 


86 


INFLAMMATION IN BONES AND JOINTS 





HEMATOGENOUS OSTEOMYELITIS 87 

more or less irregular, of course. In the later stage the new 
hone in the periosteum can be seen on the plate, and the 
sequestra surrounded by rarefied areas. 

The effusion into the neighboring joint, occasionally 
occurring in the early stages of an acute osteomyelitis, the 



Fig. 36.—Acute, suppurative, hsematogenous osteomyelitis of the clavicle, in the chronic, 

stage. 


so-called sympathetic synovitis, is usually sterile. Aspira¬ 
tion will determine this. 

An acute suppurative arthritis shows a swelling in the 
joint itself, and possibly for a short distance on each side 
of it, rather than on one side alone. Motion is much more 
painful. Fluid in the joint is an early phenomenon of 
acute arthritis, and can be found by aspiration. When 
pus is found, operation reveals its source in either instance. 

Acute inflammatory rheumatism is differentiated by 
its fleeting nature; by involvement of several joints in 







88 


INFLAMMATION IN BONES AND JOINTS 


succession, the first clearing up as the next is attacked; 
by the acid sweats; and by its reaction to salicylates. 

The severe cases, with few evidences of local disturb¬ 
ance, but with marked constitutional involvement, early 
delirium and rapidly deepening coma, offer the greatest 
difficulty. Sometimes only the necropsy clears up the 
origin of what has been diagnosed as a pyaemia of un¬ 
known origin. 

Typhoid fever has a characteristic onset, with a de¬ 
lirium usually not appearing early, intestinal symptoms, 
a Widal reaction, and an absence of leucocytosis. The 
typhoid state is rather late in typhoid. To occasion any 
confusion in osteomyelitis it would need to appear early. 

The prognosis as to life^ as well as to the time of 
complete recovery, depends largely upon the promptness 
of treatment and its thoroughness. With early operation 
the majority of patients recover. Some patients die 
quickly from toxaemia, even before the formation of pus. 
Others die after a short time from sepsis, ulcerative endo¬ 
carditis, metastases in the kidneys, etc.; others after a 
longer time from the effects of the prolonged suppuration, 
amyloid degeneration, or metastases in other bones. The 
persistence of bacteraemia after thorough drainage is a bad 
sign, but not necessarily a fatal one. 

The treatment is invariably operative, at the earliest 
possible moment, as soon as the diagnosis can be made, and 
without waiting for fluctuation. 

LTnder complete narcosis the long incision is made de¬ 
liberately in the muscle planes down to the periosteum, 
and this is slit open. If pus be found it must be followed up 
as far as it has traveled. With involvement of the marrow 
beneath, the cortex usually loses its glistening appearance 
and shows dead white, while pus, instead of blood, oozes 


HEMATOGENOUS OSTEOMYELITIS 89 

from the minute apertures of the Haversian canals. Later, 
the cortex turns a dirty brown or blackish. 

In no circumstances must fear of infecting the marrow 
induce one to stop here. A long strip of the cortex should 
be removed, the marrow canal should be inspected, and if 
it he found infected, the removal of the lid of bone over 
it should be continued until the limits of the disease have 
been reached. It is not enough to open simply the central 
marrow canal. The metaphysis, where the process started, 
must be opened as well. In the early stages the marrow 
may be found only intensely congested, perhaps with 
yellow streaks running through it; later it will consist of 
yellow or greenish pus. If we have reason to suspect 
pocketing of the pus under the periosteum on the side of 
the bone opposite to that opened, counter openings should 
be made. 

Authorities differ as to the next step. Some operators 
stop here, either leaving the wound open or stitching the 
skin to the periosteum, to ensure its staying open. Some 
curette the marrow. Some not only curette, but also pack 
the cavity. Some immediately resect all the diseased 
hone. Most operators postpone the bone removal. 
The Carrel-Dakin treatment seems particularly appro¬ 
priate after operation. 

Nichols advises that the hone be not removed until 
new bone formation in the periosteum, the involucrum, 
has well begun. This time can be determined by thrusting 
a needle into the periosteum, or more accurately by exam¬ 
ining a piece of it under the microscope. The new bone 
imparts a crackling sensation, with a slight resistance. In 
the forearm and in the leg, where the diseased bone lias a 
splint in the other bone, Nichols sets the time as about two 
months after the first operation; in the femur and in the 


90 


INFLAMMATION IN BONES AND JOINTS 


humerus, where no such splint is present, the time should 
be somewhat longer. 

Other operators wait longer before removing the 
sequestrum, but they all agree that too long an interval 
must not be allowed to elapse. If we wait too long, the 
bone in the involucrum becomes very dense. The repara¬ 
tive processes in dense bone are very poor, and in cases that 
have been postponed too long, the cavity left by the 
removal of the sequestrum may remain indefinitely. 

If early sequestrotomy be practiced, a splint should be 
applied, on account of the danger of fracture of the involu¬ 
crum, a fracture that sometimes will not unite. If time for 
the formation of a solid involucrum be permitted to 
elapse, the removal of its steep sides at operation will 
hasten healing. 

When it comes to removing the sequestrum, the dead 
bone is not as a rule found perfectly separated, but united 
at its ends to the live bone and here and there adherent to 
the periosteum. These attachments must be divided. 
Sometimes, also, a considerable amount of bone must be 
chiseled from the involucrum, to permit of the removal of 
the sequestrum. 

When the disease has involved only the superficial part 
of the cortex, the problem is much simpler. In such a case 
the sequestrum may be in the form of a long sliver of bone 
which can be removed easily. 

After the removal of the sequestrum the disease settles 
down into its chronic stage, and it is customary to allude to 
this stage as chronic osteomyelitis. It really is the stage of 
repair of the acute disease, a stage of repair which is pro¬ 
longed by mechanical conditions incident to the presence 
of the bony shell which prevents healing, as well as to the 
presence of pieces of dead bone unavoidably left behind. 


HEMATOGENOUS OSTEOMYELITIS 


91 


In favorable cases during the healing of the wound 
small sequestra are thrown out. After healing has taken 
place, to the accompaniment of slight pain and increase of 
temperature, pus pockets may form in and near the scar, 
and, rupturing, heal again after discharging small seques¬ 
tra. This may go on indefinitely, but the ordinary period 
may be said to be a year. 

The most troublesome cases are those in which, after a 
reasonable time, the processes of repair come to an end, 
leaving a cavity in the hone, with sclerosed walls, which will 
not fill in. Sometimes if the steep walls of this cavity he 
removed, giving it a shallow cup shape, repair will start up 
again, and will be completed. In other cases this procedure 
fails, especially when the cavity is near a joint, where its 
obliteration is difficult. The problem is then a difficult 
one, and has been attacked in various ways. 

Schede 7 recommended filling the cavity with an asep¬ 
tic blood clot, followed by almost complete closure of 
the wound and the application of a protective tissue be¬ 
tween it and the voluminous dressing. It is difficult or 
impossible to prevent infection of the blood clot, and in 
the hands of others than its originator, this treatment 
has not been successful. Hamilton’s 8 sponge graft seems 
to have no advocates nowadays, nor Senn’s 9 decalcified 
bone chips. 

Good results have been obtained with Neuber’s 10 oper- 

7 Schede: “Ueber die Heilung unter dem feuchten Blutschorf.” Dtsch. 
med. Wochensch., 1886, xii, 389. 

8 Hamilton, D. J.: “On sponge grafting.” Edin. Med. Jour., 1881, xxvii, 

385. 

9 Senn, Nicholas: “Healing of aseptic bone cavities.” Am. Jour, of 
Med, Sci., 1899, xcviii, 219. 

10 Nettber : “Zur Behandlung starrwandigen Hbhlenwunden.” Arch. f . 
klin, Chir., 1896, li, 683. 




92 


INFLAMMATION IN BONES AND JOINTS 


ation. Neuber cleaned out the bone cavity, .trimmed off 
its steep walls as much as possible, and turned in flaps of 
skin and soft tissue, securing them to the bone by nails, 
straps and invagination sutures. 

Perhaps the most promising procedure is, after trim¬ 
ming the walls of the cavity and rendering them, as far as 
possible, aseptic, to fill them with some special form of 
paste. The exact chemical combination of the paste is 
probably not a matter of great importance. As von 
Mosetig-Moorhoff 11 says, the “ plombe ” is merely a tem¬ 
porary substitute. Von Mosetig-Moorhoff, after thorough 
disinfection and drying of the walls of the cavity, filled it 
with a paste composed of a sterile mixture of iodoform 40 
parts, and oil of sesame and spermaceti 30 parts each. He 
then closed the wound. 12 

The treatment of the superficial form of the disease is 
usually much simpler than that of the preceding. As a 
rule only the superficial portion of the bone is killed, and 
this only in a limited area. Healing follows slowly after 
the removal of the dead bone. 

The Circumscribed Form or Osteomyelitis— 
Brodie^s Abscess. —The abscess should be cleaned out 
thoroughly, and its sclerosed walls should be chiseled 
away. The employment of some paste may be advisable to 
promote the healing in of the cavity, e.g., Mosetig- 
Moorhoff’s, Beck’s or “ bipp.” The formulae of Beck’s two 
pastes are: No. 1, bismuth subnitrate (arsenic free) 33 
per cent., vaselin 67 per cent. No. 2, bismuth subnitrate 
30 per cent., vaselin 60 per cent., paraffin (120° melting 
point) 5 per cent., white wax 5 per cent. The formula for 

11 Vox Mosetig-Moorhoff, Dr. R.: “The elimination of cavities in opera¬ 
tive wounds.” Surgery, Gynecology and Obstetrics, 190G, iii, 547. 

12 See also Cxopton, M. B.: “The diagnosis and treatment of osteomy¬ 
elitis.” Surgery, Gynecology and Obstetrics, 1915, xx, 6. 





HEMATOGENOUS OSTEOMYELITIS 


93 


bipp is: Iodoform 16 ounces, bismuth subnitrate 8 ounces, 
liquid paraffin 8 fluid ounces, or a sufficient quantity. If 
Beck s paste or bipp be used, one must be on the lookout 
for symptoms of bismuth poisoning. 1 " The possibility of 
iodoform poisoning with bipp and Mosetig-Moorhoff’s 
pastes must not be forgotten. Perhaps vaselin and 
paraffin, without iodoform and bismuth, would be as effi¬ 
cacious as with them. 

In operations on old sterile bone abscesses, the wound 
may be closed immediately. 

13 Beck, Emil G.: “Bismuth paste in chronic suppuration.” St. Louis 
C. V. Mosby Co., 1915, 182. 

Dreesmanx: “ Ueber Wismuthvergiftung.” Miincli. pied. Wchnschr., 
1901, xlviii, 238. 

Ely, Leonard W.: “A fatal case of bismuth paste poisoning.” Med. 
Record, 1912, lxxxi, 119. 

Freilich, Ellis B.: “Bismuth poisoning following bismuth paste injec¬ 
tion.” J. A. M. A., 1917, lxviii, 111. 

Mayer, Leo, and Baehr, George: “Bismuth poisoning.” Surf/., Gynec. 
and Obst., 1912, xv, 309. 

Morison, Rutherford: “The treatment of infected suppurating war 
wounds.” Brit. Jour. Surg., 1916-17, lv, 660. 

Muiilig, F.: “Ueber Wismuthvergiftung.” Munch. Med. Wchnschr., 1901, 
lxviii, 592. 

Sigmund, Erdheim: “Ueber Wismutintoxikation bei Behandlung nach 
der Methode von Beck.” Wien. klin. Wchnschr., 1912, xxv, 749. 

Vaccarezza, Raul F.: “Las intoxicaciones por el subnitrato de bismuto.” 
La Semana Med., 1919, xxvi, 366. 



CHAPTER II 



ACUTE SUPPURATIVE HHEMATOGENOUS ARTHRITIS 

The Articular Form.— It is quite likely that the 
infectious material may be carried to the synovial mem¬ 
brane in the first place, and thus that a suppurative 


arthritis may precede the osteomyelitis, or may exist alone 
without involvement of the bone. The result in either case 
is much the same, though if the synovial membrane alone be 

affected, the treatment may be different. 

94 


Fig. 37. —Photomicrograph of bone and cartilage from a section of 
acute suppurative arthritis, following operation on a case of suppu¬ 
rative inflammation on the shaft of the tibia. Degenerating cartilage 
on the right, bone marrow on the left. Observe how the inflamma¬ 
tory process in the marrow is eating its way into the cartilage, and 
how it has already consumed most of the bone Only a few small 

trabeculae are left. 



95 


HEMATOGENOUS OSTEOMYELITIS 

In the treatment of these acute suppurative arthritides 
the problem is not, as in an uncomplicated osteomyelitis, a 
simple one of thorough drainage, but we are led to take 
risks by the hope of a movable joint. Again, in the case of 



Fig. 38. —Suppurative inflammation in the bone marrow in the region of the joint. T, T, T 
trabeculae; C, colony of pus cocci in a small vessel. We know that in this case the bone is rapidly 
being destroyed, but the margins of the trabeculae present an appearance typical of what is 

usually described as productive ostitis. 

a child, we must not do any more injury than is absolutely 
necessary to the epiphysial cartilage. 

Thorough drainage is demanded here as in the other 
forms of the disease, but it is well not to be too radical 
about gouging out the bone, especially about the epiphy- 





96 


INFLAMMATION IN BONES AND JOINTS 


sial cartilage. If constitutional symptoms be not severe, 
and if aspiration of the joint have revealed only a few leu¬ 
cocytes or even a few cocci, we may postpone opening it, 
possibly following Murphy’s advice, 1 washing it out and 
injecting its cavity with a 2 per cent, solution of formalde¬ 
hyde in glycerin. The injection may perhaps be repeated 
once or twice if the constitutional symptoms and the local 
physical signs justify it. 

If the joint be full of pus, containing many cocci, little 
is to be gained by temporizing. It should be opened and 
thoroughly drained. Any drains which we insert must be 
left in, of course, as long as necessary, and yet we must 
remember that joints which have had tubes in them for any 
length of time usually become ankylosed. On the other 
hand, it is not likely that a joint, invaded by an osteo¬ 
myelitis in the vicinity serious enough to damage the 
cartilage badly, will ever possess enough function to 
justify much risk for its preservation. Cartilage scraped 
off from limited areas of the articular surface of animals’ 
bones sometimes reforms, but nothing that I have ever 
seen in my specimens makes me think that it is replaced 
after it has been destroyed by disease. We come back, 
then, to the principle that an acute hematogenous sup¬ 
purative arthritis requires free drainage. 

In disease of the knee or hip, traction may promote the 
comfort of the patient, and possibly may help in the treat¬ 
ment. Later on some such splint as the Thomas may be 
of service when the lower extremity is affected. 

It is sometimes impossible in an acute hematogenous 
suppurative arthritis to decide whether the synovial mem¬ 
brane alone is involved or whether the infection springs 

1 Murphy, John B.: “Metastatic gonorrheal arthritis of the knee.” 
Surgical Clinics of John B. Murphy ; 1912, i, 825. 



HEMATOGENOUS OSTEOMYELITIS 


97 


from a marrow focus in the immediate vicinity. If the 
bone involvement is so minute as to escape detection, it 
may be ignored. 

A suppurative hematogenous arthritis is occa¬ 
sionally caused by the diplococcus of pneumonia. The 
disease comes on during a pneumonia or in early conva¬ 
lescence, and is often fatal." It may arise in the course of 
a general infection, and very rarely it is primary. Its 
treatment is the same as that of the preceding, but cures by 
aspiration have been reported. If the constitutional 
symptoms warrant it, this should be tried before more 
radical measures. 

A hematogenous arthritis occasionally is observed 
as a sequel of certain acute infectious diseases, notably 
scarlet fever, measles, smallpox and influenza. 2 3 The 
inflammation may consist of a mild synovitis, single or 

2 Bezancon, F. and Griffon, V.: “Arthritis experimentales a pneu- 
mocoques par infection generale et sans traumatisme articulaire.” Soc. d. 
Biol. Comp. Rend., 1899, li, 709. 

Cave, Edward J.: “ Pneumococcic arthritis.” Lancet, 1901, i, 82. 

Dunn, L. A. Robinson, H. Betiiam and Fletcher, II. Morley: “ Five 
cases of purulent pneumococcic arthritis in children.” Lancet, 1903, ii, 316. 

Ely, Leonard W.: “A case of pneumococcus infection of the hip.” Med. 
News, 1905, lxxxvi, 930. 

Herrick, James B.: “Pneumococcic arthritis.” Am. Jour. Med. Sci., 
1902, cxxiv, 12. 

Horsfall, C. E., Campbell: “Pneumococcus arthritis; vaccine treat¬ 
ment; recovery.” Lancet, 1918, ii, 556. 

Pasteur, W. and Courtauld, L.: “Primary pneumococcal arthritis.” Lancet, 
1906, i, 1747. 

Raw, Nathan : “ Pneumococcus arthritis with notes of seven cases.” Brit. 
Med. Jour., 1901, i, 1803. 

Secretan, W. Bernard, and Wrangiiam, William: “Pneumococcic 
arthritis.” Brit. Med. Jour., 1906, i, 915. 

3 Fritschs “ Ueber Gelenkerkrankungen hie Scharlach und Masern.” Beit. z. 
klin. Chir. 1911, lxxii, 101. 

Schueller, Max : “Ueber Bacterien bei metastatischen Gelenkentziind- 
ungen.” Archiv. f. klin. Chir., 1884-5, xxxi, 276. 


7 



98 


INFLAMMATION IN BONES AND JOINTS 


multiple, which soon clears up entirely, or it may be more 
severe, with a plastic exudate. This latter form is fre¬ 
quently seen after influenza, and may result in almost 
complete ankylosis, from the dense adhesions in the joint. 
The arthritis may be suppurative, and not to be distin¬ 
guished from the acute streptococcic form already 
described. Its treatment is the same. 


CHAPTER III 


SUPPURATIVE OSTEOMYELITIS FOLLOWING 
COMPOUND FRACTURE 

The suppurative osteomyelitis which follows infection 
from a compound fracture differs in its course and in its 
clinical manifestations from the hasmatogenous form, but 
the fundamentals of the pathological process of the two 
are much the same. The infection, of course, is always a 
mixed one, and, starting from any part of the bone, it 
spreads in every direction. In former days it was fre¬ 
quently fatal, but since the introduction of the modern 
methods of treatment of compound fractures, except in 
war wounds it is rarely seen. Otherwise its manifestations 
are often mild in their nature. 

The treatment in the first place is prophylactic. A 
compound fracture which is considered clean may be 
treated expectantly, but at the first sign of infection, it 
should be thoroughly opened up. All foreign material 
and necrotic or loose bone fragments should be cleaned out, 
but bone fragments still attached to the periosteum should 
be left. Their presence is said to promote the union of the 
fracture. Provision should be made for drainage, and pos¬ 
sibly some form of wound disinfection should be installed— 
Carrel-Dakin. If in spite of our efforts, the infection 
spread, amputation may be necessary. 

Non-union frequently follows infected compound 
fractures. It is well not to undertake any operation for 
this until after the wound has been healed for several 
months. Otherwise we run the risk of lighting up the 
infection afresh. 


99 


CHAPTER IV 

TYPHOID OSTEOMYELITIS AND ARTHRITIS 


Typhoid Osteomyelitis. —It appears from the inves¬ 
tigations of Fraenkel 1 and others that the bone marrow is 
a favorite domicile of the typhoid bacillus, after clinical 
recovery as well as during the actual course of the disease. 
Sometimes it causes an osteomyelitis which is wont to 
affect the superficial jiortion of the cortex, and may or 
may not result in suppuration, The infection may be a 
simple one or it may be mixed. The shafts of the long 
bones, especially of the ribs or of the tibia seem to be 
affected by preference, but the disease is by no means rare 
in the spine. It is commonly called a periostitis when it 
occurs in the shafts of the long bones. 

Typhoid osteomyelitis usually develops in the third or 
fourth week of the disease, or at any time after the typhoid 
has run its course, and its onset is manifest ordinarily by a 
rise of temperature and a painful swelling of the bone. If 
suppuration results, the abscess should be thoroughly 
cleaned out and drained. The milder cases of a pure 
typhoid infection often disappear spontaneously, and need 
no other treatment than rest and protection from injury. 

TYPHOID ARTHRITIS 

An arthritis is an occasional complication of typhoid 
fever, coming on in the late stages of the disease, or during 
convalescence. The fluid in the joint may be sterile, or it 
may contain typhoid bacilli, alone or mixed with pus cocci. 2 

1 Fraenkel, Eug.: “ Ueber Knochenmark and Infektionskrankheiten.” 
Muenchener medicinische Wochenschrift, 1902, xlix, 561. 

2 Ellis, A. G.: “As Experimental Study of Joint Affections Induced by 
the Typhoid Bacillus,” Jour, of Infect, Dis, } 1909, vi, 181. 

ioo 






TYPHOID OSTEOMYELITIS AND ARTHRITIS 101 

Marrow involvement is probably, as a rule, slight. The 
chief pathological changes appear to be in the syno¬ 
vial membrane. 

Typhoid arthritis most often occurs in the hip, and 
usually is not very painful. Dislocation of' the hip is a 
rather frequent result. 

The treatment consists in rest and protection. In 
order to avoid a dislocation of the hip, the attitude of ex¬ 
treme flexion and adduction is to be avoided. If the joint 
be much distended with fluid it should be aspirated. With 
secondary infection by pus germs an operation becomes 
necessary, though, as the infection is probably synovial 
alone, it may possibly be checked by washing out the joint 

cavity with normal salt solution, and then injecting it with 
* 

a mild antiseptic such as a solution of formaldehyde. 

Typhoid spine. —This is an acute affection of the 
spine, coming on in the late stages of a typhoid, or during 
convalescence, and generally in vigorous young men. Its 
pathology has not been definitely established, for no case 
ever has come to necropsy, though in Hugh s case a 
necropsy was done nine years after the attack. Oslei 
taught for many years that it was a neurosis, but the 
clinical picture, the Rontgen plate, and the occurrence of 
a kyphosis in one or two cases indicate that it is essentially 
an osteomyelitis, perhaps with an arthritis as well. No case 
ever has gone on to suppuration, and we assume that the 
offending organism is the typhoid bacillus. 

The disease may be mild and insignificant, and may 
pass as a “ lumbago ” practically unnoticed; it may be very 
severe. Its onset may be sudden or slow. Usually, in the 
late stages of a typhoid or during convalescence, the patient 



102 


INFLAMMATION IN BONES AND JOINTS 


complains of stiffness in his back and of pain in the lumbar 
region. The pain in the severe cases is horrible, and is 
increased by the slightest motion. The patient is unable 
to turn in bed and cries out if the bed is only slightly jarred. 

The pain often comes in paroxysms, preceded perhaps 
by a rise in temperature. It may remain localized in the 
back, or it may run around the abdomen, or into the ex¬ 
tremities. It may shift. 

With the symptoms of an actual bony lesion may go 
those of a neurosis, or even of a marked hysteria—pares¬ 
thesias, muscular contractions, changes in the reflexes, etc. 

After a longer or shorter interval the symptoms slowly 
subside, and the patient recovers completely within a year. 
The milder cases run a short course. 

The treatment may be summed up in one word— 
rest. The severe cases demand recumbency, possibly with 
the immobilization reinforced by a gas-pipe frame, covered 
with canvas, to which the patient is strapped. Morphine, 
or even a whiff of chloroform or of ether may be necessary 
to quiet the paroxysms of pain. 

For the milder cases, and for the later stages of the 
severe ones, sufficient immobilization is furnished by a light 
steel spinal brace, or by a plaster jacket. The white-hot 
thermo-cautery, flicked quickly over the lumbar region, 
relieves the late pain and stiffness, and its application is 
relished by the patient. 


CHAPTER V 


GONOCOCCIC OSTEOMYELITIS AND ARTHRITIS 

The gonococcus can cause an inflammation of the bone 
marrow, or of the synovial membrane, or of both. Practi¬ 
cally all authorities speak of a gonorrheal periostitis. I 
believe that this is not correct. The inflammation is in 
the superficial portion of the bone marrow and not in 
the periosteum. 

On account of the difficulty of recovering and growing 
the gonococcus, our observations on the disease are largely 
clinical. The corollary to this is that much difference of 
opinion prevails in regard to the disease. The cause of 
gonorrheal arthritis is of course the gonococcus, but the 
diagnosis is made far more often without the demonstra¬ 
tion of the organism than with it. The disease, as would be 
expected, seems to be more common in men than in women. 

It is customary to speak of acute and of chronic gono¬ 
coccic arthritis and to teach that while its incidence is 
usually in the florid stage of the urethral infection, at about 
the time of invasion of the deep urethra, it may nevertheless 
come on at any time during the course of an old chronic 
infection in the deep urethra. I think that this is an error; 
that a gonococcal arthritis is always an acute arthritis, and 
that it almost invariably, if not invariably, comes on during 
the acute stage of the urethral infection. I have never seen 
the gonococcus recovered from a case of chronic arthritis, 
and believe that in the old cases of chronic arthritis caused 
bv a lesion in the deep urethra, the streptococcus is the 
offending organism. Baer, 1 however found the gonococcus 

1 Baer, W. S.: “Painful heels.” Johns Hopkins Hospital Bulletin, 1905, 
xvi, 264. 


103 





104 


INFLAMMATION IN BONES AND JOINTS 


in a number of old spurs under the calcaneus. In acute 
arthritis the organism has a fleeting life; one day aspiration 
of the joint, especially immediately after an acute exacer¬ 
bation, detects it; the next day it may be gone. One might 
take either side of a wager on its presence or absence. 

On account of a paucity of pathological material we 
know little of the finer changes in the bone and joint. In 
the region of the joint the bone usually shows rarefaction 
under the X-ray. Farther from the joint, immediately 
under the periosteum, bone absorption and bone production 
go hand in hand. This often results in irregular spurs 
and exostoses. 

The synovial membrane is inflamed, succulent, con¬ 
gested and villous. The exudate in the joint, while 
occasionally purulent or possibly serous, usually is fibrinous 
or plastic. It results sometimes in dense fibrous adhesions, 
which limit or abolish joint motion. 

The typical and characteristic invasion of the disease, 
not by any means invariable, however, is as follows: For 
a day or two several joints swell up and become slightly 
painful, one clearing up as the next is involved. Then, 
suddenly, the disease attacks one or perhaps two joints and 
stays there. The swelling and pain are great, with an 
increase of local temperature and marked sensitiveness. 
The joint is distended with fluid. (Edema of the tissues 
in the neighborhood may be said to be almost characteristic. 
Constitutional symptoms as a rule are not marked. High 
fever with pronounced constitutional symptoms, usually 
spells mixed infection. 

The large joints are more frequently involved than the 
small ones. Everyone has his own ideas as to the relative 
frequency of involvement of the various joints. Person¬ 
ally I look for it in the man most often in the knee or ankle. 


GONOCOCCIC OSTEOMYELITIS AND ARTHRITIS 105 

in the woman most often in the wrist, hut then 1 have not 
seen many cases in which I was sure of the diagnosis. 
Sterno-clavicnlar involvement is most suggestive of 
the gonococcus. 

The disease has no definite course. Recovery may take 
place after a longer or shorter time, either complete or with 
much or little remaining stiffness. Endocarditis, iritis and 
“gonococcic septicaemia” accompany the arthritis quite 
frequently, possibly because they all are an evidence of a 
severe infection, or of a high degree of vulnerability on the 
part of the patient. 

The diagnosis as a rule is not difficult. The presence 
of an acute urethral infection is strong presumptive evi¬ 
dence. The patient rarely attempts to hide this, as he does 
a chronic one. Acute inflammatory rheumatism has a fleet¬ 
ing nature, acid sweats, and usually a ready reaction to the 
salicylates. In acute suppurative hematogenous osteomy¬ 
elitis the start of the process is outside the joint. From 
acute suppurative hematogenous arthritis the disease may 
be differentiated by aspiration. The fluid from a gono¬ 
coccic joint is sterile or contains gonococci. 

Treatment. —Some authorities recommend immobil¬ 
ization, others maintain that immobilized gonococcic joints 
are more likely to become ankylosed. Hot applications are 
grateful to some patients, cold applications to others. 
Good results have followed washing out the joint with 
normal salt solution, or with a solution of protargol 
or argyrol. 

In aspirating or washing out a joint it is well to incise 
the skin and superficial fascia with a scalpel, and then use 
a large calibre needle or a trocar. 

Specific antigonococcic sera and vaccines have been 
employed often during the past ten years, and have been 


106 


INFLAMMATION IN BONES AND JOINTS 


highly praised. Apparently they are of great value. Re¬ 
cent investigations, however, indicate that the specificity 
is of no importance. The result of the use of non-specific 
proteins is said to equal that of specific proteins. 

Whatever local treatment be instituted, the prime indi¬ 
cation in these cases is the treatment of the primary focus 



Fig. 39.—The so-called gonorrheal periostitis of the tubercle of the calcaneus. 

in the genito-urinary tract. It is a strange thing that the 
urethral symptoms often lessen as the joint becomes in¬ 
volved, to reappear as the joint condition improves. 

A peculiar condition sometimes is seen in old cases of 
deep urethral infections. The patient complains of pain 
in the soles of his feet, where the plantar fascia is inserted 
into the tubercle of the calcaneus. Standing and walking 
are painful. Pressure by the thumb brings out the sensi¬ 
tiveness very prettily. The gait is characteristic. The 


GONOCOCCIC OSTEOMYELITIS AND ARTHRITIS 107 

patient walks as if he were treading on eggs. The Rontgen 
rays may or may not show a roughening of the calcaneal 
tubercle. Baer recovered the gonococcus from the tubercle 
in one or two cases. 

Attention to the lesion in the deep urethra usually 
causes a prompt disappearance of the symptoms. Vesicu¬ 
lotomy is often necessary. Massage of the prostate may 
be tried. Possibly strapping, or a sole plate sharply 
arched up under the anterior part of the calcaneus, may 
also be of benefit. 

Some surgeons advise an operation. The incision may 
be made on the medial aspect of the heel. It is carried down 
to the bone, and the suspected tissue is scraped out. Opera¬ 
tion is rarely necessary if the deep urethra be cleared up. 

A similar condition of painful heels, not so marked nor 
so characteristic, is occasionally observed in patients with 
a focus of infection in their teeth or tonsils. Patients with 
flat feet also may complain of painful heels, but they have 
not the “egg-walking” gait. A spur is occasionally seen in 
the Rontgen picture of normal calcanea. It gives no 
symptoms, and requires no treatment. 


CHAPTER VI 

ACUTE INFLAMMATORY RHEUMATISM 


Strictly speaking, this is not a joint disease, but a 
general disease characterized by painful joint swellings and 
a marked pyrexia. Its cause never has been demonstrated. 
Numerous investigators 1,2,3,4,5 ’ 6 ’ 7 ’ 8 ’ 9 ’ have isolated organ¬ 
isms from the blood and from the joints, but 
have not succeeded in proving their causal relationship. 
Some believe that the disease is a toxaemia or a mild 
form of pyaemia. A modern view is that it is essentially 
an anaphylactic reaction, similar to that, for instance, 
against diphtheria antitoxin, but more severe. A strong 
array of evidence points to the tonsil as the seat of the 
infection, whatever it may be. 


Acute inflammatory rheumatism is characterised by a 

^_ •/ 

AchalmEj P.: Sur un signe de diagnostic precoce des attaques et 

des rechutes de rhumatisme articulaire aigu.” Arch. Gen. de Med., 1902. cxc 

257. 


Beaton, R. M., and Walker, E. "W. A.: 44 The Etiology of acute rheu¬ 
matism and allied conditions.” Brit. Med. Jour., 1903, i, 237. 

3 Beattie, James M.: “A contribution to the bacteriology of rheumatic 
fever.” Brit. Med. Jour., 1906, ii, 1781. 

4 Beattie, James M.: “The Micrococcus rheumaticus. . ,” Brit. Med. 
Jour., 1904, ii, 1511. 

Lewis, Morris J., and Loncope, W t arfield T.: “ Experimental Arthri¬ 
tis and endocarditis...” Assn. Am. Pliys. Trans., 1904, xix, 457. 

6 Poynton, Frederick J., and Paine, Alexander: “The etiology of 
rheumatic fever.” Lancet, 1900, ii, 861, 932. 

Poynton, F. J., and Paine, Alexander: “Some further investigations 
and observations upon the pathology of rheumatic fever.” Lancet, 1910, i, 1524. 

8 Rosenow, E. C.: “The Etiology of acute rheumatism, articular and 
muscular,” Jour. Infec. Bis., 1914, xiv, 61. 

0 Triboulet and Coyon : “ Recherches bacteriologiques concernant un 
cas de rheumatisme febrile mortal. . ” Soc. de Biol, Corny. Rend., 1897, xlix, 
1000 . 


108 




ACUTE INFLAMMATORY RHEUMATISM 109 

high, irregular, remittent temperature, a high colored acid 
urine, and sweats. The larger joints as a rule, suffer most. 
They swell, one after another, and are exquisitely sensitive 
to motion and to touch. The swelling is circumarticular as 
well as articular. The adjacent tendon sheaths may also 
be involved. The joint is red and hot. The great peculi¬ 
arity of the disease is its fleeting nature. It flits from 
joint to joint, one joint clearing up as the next becomes 
involved. Another marked feature is its reaction to 
the salicylates. 

Acute inflammatory rheumatism is rarely overlooked 
when it is present. Its features are so characteristic that 
they can hardly be ignored. The diagnosis is employed 
too often rather than too seldom. Many lives have been 
lost by failing to recognise an acute suppurative arthritis, 
and treating it as “ rheumatism.” It is a good rule never 
to diagnose anything as rheumatism, until every thing 
else has been ruled out. 

The treatment belongs in the realm of internal 
medicine. Splinting may alleviate the pain. There is a 
history of frequent sore throat, and the tonsils are diseased. 
These organs should be removed. Not infrequently the 
disease lights up after tonsillectomy, probably on account 
of the entrance of organisms through the raw surface. 


CHAPTER VII 

HYDRARTHROSIS INTERMITTENS 


Intermittent Synovitis, Intermittent Joint Hydrops 

This rare and somewhat mysterious lesion was de¬ 
scribed by Perrin . 1 It consists of a periodic effusion into 
one or more joints, usually into the knee. The fluid re¬ 
mains for a few days and then disappears. 

The cause is unknown. It has been regarded as a 
syphilitic manifestation, as a neurosis, and as a reaction of 
the synovial membrane to a focus of infection in the end of 
the bone, or in some other part of the body. Coincident 
disease of the thyroid gland has been noted, and vasomotor 
disturbances elsewhere. Some observers consider it as a 
passive effusion, others as a synovitis. It occurs with about 
equal frequency in men and women. 

The joint fluid is usually serous, and contains flakes of 
fibrin. The synovial membrane shows its customary reac¬ 
tion to the presence of fluid in the joint cavity, and becomes 
thickened and villous. 

The swelling usually comes on rather suddenly, in¬ 
creases for a few days, and then subsides, to return after 
an interval which may vary in length. Pain, if present, 
is not usually severe. Fever, dizziness, headache, pain in 
the limbs, vasomotor disturbances and other constitutional 
symptoms have been observed. In women a certain relation 
to the menses has been noted. If several joints are attacked, 
they may be attacked coincidently or one after another. 
Occasionally the affection leaves one joint and attacks an- 

1 Perkin: Journal de Medecine. Par. 1845, iii, 82. 


IIO 




HYDRARTHROSIS INTERMITTENS 


111 


other, like acute inflammatory rheumatism. Sometimes 
the patient can foretell the exact date of his next attack, 
but again cases which have been regular in their recur¬ 
rence may become irregular, and vice versa. In women 
the attacks sometimes have subsided during pregnancy. 

Treatment. —Immobilization, apparently, is of no 
avail. As to internal medication the best results seem to 
have been obtained with quinine and arsenic, although no 
malarial basis ever has been found for the disease. On the 
chance that it may be caused by a focus of infection in the 
bone end, or possibly may be an “anaphylaxis ’ to a distant 
focus, a search for a focus should be instituted, and if one 
be found, it should be removed. The only patient with this 
affection I ever saw, had evidences of infection in both teeth 
and tonsils, whose eradication she would not permit. 



CHAPTER VIII 


TRAUMATIC ARTHRITIS 
Traumatic Synovitis 

A simple traumatic arthritis may be caused by an in¬ 
jury to the joint capsule, or by an intraarticular fracture. 
In either case blood is poured out into the joint cavity, and 
probably, by its mere presence, irritates the synovial mem¬ 
brane. The membrane becomes thickened, infiltrated, 
succulent and villous, encroaching somewhat on the carti¬ 
lage at its border. When the effusion has been absorbed, 
and the capsule or bone has healed, the synovial membrane 
returns to normal. A bloody or fibrinous exudate often 
leaves adhesions behind, with some stiffness which persists 
for a while. 

The diagnosis is usually quite simple. An acute 
arthritis immediately following an injury is practically 
always a traumatic arthritis. It is not always easy to dif¬ 
ferentiate between the injury to the capsule—a sprain— 
and one to the bone—a fracture. Excluding the Rontgen 
rays, perhaps the two most valuable helps are the ecchy- 
mosis and the point tenderness on the bone in fracture. 
False point of motion and crepitus are hard to elicit unless 
the fracture is a severe one, and then there will be little 
difficulty in the diagnosis. 

The treatment of the arthritis complicating fracture 
is that of the fracture itself, except that if the amount of 
fluid in the joint be excessive, and cause great pain and 
possibly difficulty in the reduction of the fragments, it may 
be aspirated under strict asepsis. 


112 





TRAUMATIC ARTHRITIS 


113 


The continued pain and stiffness which follow the 
healing of a fracture with misplaced fragments in a healthy 
person, are probably due to the constant spraining of the 
damaged joint apparatus, viewed as a machine. It is 
doubtful if any permanent changes are set up in the bone 
thereby. If, for instance, from an old stiff wrist, following 
a carpal fracture, the offending fragments be removed, 
good function often returns. On the other hand, marked 
stiffness and disability frequently follow a well reduced 
fracture, especially in an elderly person. In such case a 
careful examination of the patient, and especially of his 
other joints will probably reveal evidences of preexisting 
hone changes. It is likely that the fracture simply con¬ 
verted a walled-in chronic infectious osteomyelitis into a 
chronic arthritis, which will be improved by prompt atten¬ 
tion to the teeth. 

A sprain is the tearing of a ligament, but the term in¬ 
cludes also the traumatic arthritis which results, and in the 
knee this is so dominant that we are wont to allude to the 
injury as a synovitis, whereas in the ankle we never should 
think of calling it anything but a sprain. 

The cardinal symptoms are pain and restriction of 
motion, especially of motion in one direction. The joint is 
swollen and its contour is changed. It contains fluid, which 
can easily be demonstrated in the knee and in the elbow, 
with more difficulty in the hip, ankle and spine. In the 
knee, the fluid floats the patella off the condyles; in the 
elbow fluctuation is to be sought posteriorly at the sides of 
the triceps tendon. The pain is made worse by motion 
which puts the damaged ligament on the stretch. Usually 
the joint is held in semiflexion. 

The diagnosis with the help of the Rontgen rays 
usually is simple. Without it, it is often impossible. The 
8 


114 


INFLAMMATION IN BONES AND JOINTS 


main thing to establish is that the joint was normal at the 
time of the injury, in order that one may exclude a disease 
that was simply aggravated by it. 

Treatment. —The first indication is to restrict as much 
as possible the formation of the exudate in the joint, 
especially in a joint that has a capacious cavity like the 
knee. This is done by rest, pressure, strapping, bandaging 
on a splint, etc. Ice bags, or hot compresses also are use¬ 
ful. These measures may be continued for a few hours. 
Later the important indication is rest, not necessarily rest 
for the whole joint, but rest for its damaged paid. In the 
later stages, to overcome stiffness, physical therapy 
—baking, hydrotherapy, massage—may occasionally 
be advisable. 

The knee is usually sprained in its medial ligament, 
and especially when it is in flexion. Far less often is a 
crucial ligament torn. Therefore the chief indication, 
after the acute symptoms have subsided, is to hold the 
joint in extension, in which position it is rarely injured. 
This is accomplished by diagonal criss-cross strapping 
with overlapping strips of adhesive plaster about ten inches 
in length and an inch or two in width, quite firmly applied 
over the front and sides of the knee, reaching from a point 
below the joint to one above the top of the quadriceps 
pouch. This strapping not only prevents flexion but also 
exerts pressure. The patient is encouraged to go about, 
preferably with a cane. His comfort is a good indication 
of the efficacy of the treatment. If he suffers pain the 
treatment is not sufficient. Then immobilization probably 
will be necessary, and subsequent physical therapy. 

If a semilunar cartilage be torn, the semidetached piece 
becomes pinched between the tibia and femur, and the joint 
is sprained. It fills with fluid, and an attack of “synovitis” 





TRAUMATIC ARTHRITIS 


115 


results. Often the knee Mocks'' in semifiexion, and only 
can be released by manipulation by the patient himself or 
by a bystander. Sometimes the deformity is fixed, and 
cannot be overcome. When the knee has been straightened, 
it usually swells for a while and is painful. The symptoms 
slowly subside, and the j oint returns to normal. No further 
trouble may be experienced, but as a rule the accident re¬ 
curs, possibly many times, and each time it is followed by 
the symptoms of joint irritation, usually not so severe as 
those following the first attack. The cause is a twist of the 
knee when it is in semiflexion. It is a frequent accident 
among athletes, especially among football players. The 
medial meniscus is much the more frequently torn. 

The diagnosis as a rule is not difficult. The Rontgen 
picture is negative. The patient gives the history of the 
attacks of locking. If sensitiveness of the anterior portion 
of the medial meniscus be present in addition, the diagnosis 
is fairly certain, though surgeons who have often opened 
the knee agree that absolute certainty is not possible. 

Treatment. —Various manipulations by the patient 
are successful in reducing the deformity—shaking the leg 
on the thigh, while the patient is erect or lying on his face, 
swimming motions carried out on the floor, etc. The 
surgeon may aid by shaking the flexed leg with the patient 
prone, or by flexing, extending and rotating. Jones 1 
recommends “ acute flexion, lateral deviation, and rotation 
inwards and full extension.” Sometimes it is hard to tell 
whether the cartilage has been reduced or not. The patient 
may be able to give us the required information, but there 
is a peculiar feel that may clinch the matter. If, with the 
patient supine, the knee be passively flexed and extended, 
attempted full extension comes to a sort of springy stop as 

Mones. Robert: “Notes on derangement of the knee.” Annals of Surg 

1909, i, 969. 



116 


INFLAMMATION IN BONES AND JOINTS 


long as the cartilage is out of place, whereas with a normal 
knee, the stop is sudden and definitive. If all attempts at 
reduction fail, it is sometimes wise to send the patient home 
for 24 hours, to see what lie can do by himself. If he fail, 
operation is practically imperative. 

When the cartilage is first torn and has been reduced, 
the knee should be splinted, at least partially, and should be 
treated with the idea of healing the torn cartilage. There 
is a reasonable chance of success by these means. With 
each succeeding slip the chances grow smaller. Most 
authorities agree that recovery is not to be expected after 
the cartilage has been out two or three times, but cases have 
been observed (I have had a personal experience with one) 
in which recoverv has ensued after numerous attacks. This 
is rare, and there is alwavs an element of risk in the acci- 
dent. There are times when a simple fall in the street from 
locking of the joint might be fatal. Most surgeons do not 
operate after the first slip, especially as the diagnosis is not 
a matter of certainty. The oftener the accident recurs 
after this, the stronger is the indication for operation. 

Jones’s operation, with the knee flexed, has attained 
a wide popularity. Strict asepsis is of the first importance. 
Not even a gloved finger should touch the wound. All 
sponges should be on holders. Artificial ischaemia is to be 
employed. The patient’s legs hang over the end of the 
operating table, and the operator sits facing them. 

The incision is a curved one. It starts from a point just 
proximal to the distal border of the patella, and about a 
centimetre medial to its medial border, runs distally to a 
point about a centimetre distal to the tibial margin, and 
then curves sharply medialwards for about two centimetres. 
It is about eight centimetres long. The incision through 
the capsule is about half as long. The edges of the wound 


TRAUMATIC ARTHRITIS 


117 


are retracted, and the torn piece of cartilage is cut off with 
a knife, and without traction on it. Jones never ties ves¬ 
sels, always uses a tourniquet, and never drains. The 
wound is sutured in layers. The joint is immobilized for 
eight or ten days, and then passive motion and massage 
are begun. 

The ankle is usually sprained by a twist of the foot 
inward, tearing the external lateral ligament. An excel¬ 
lent treatment, perhaps after twenty-four hours of hot or 
cold applications, is that with the Cottrell (sometimes 
erroneously called the Gibney) strapping. 

Treatment. —The foot is held in dorsal flexion and 
marked eversion. The plaster, in strips one inch wide, and 
in two lengths, eight and twelve inches, is to be ready at 
hand. The first strap (eight inch) starts just behind the 
metatarsophalangeal joint of the little toe, runs around 
behind the heel, and ends in the region of the medial mal¬ 
leolus. The second (twelve inch), starts about the middle 
of the lateral surface of the calf, passes down the leg, under 
the heel near its posterior part, and ends near the medial 
malleolus. The third overlaps the proximal half of the 
first, the fourth the anterior half of the second, and so on 
until about eight have been applied. A few criss-cross 
straps reinforce these where they cross at the ankle, and a 
snug bandage holds them all in place. The immediate 
relief afforded by this dressing is often remarkable, when 
it is properly applied. 

Sprain of the elbow is rare and demands rest. The 
same may be said of the shoulder. Subacromial bursitis, 
with its painful rotation and abduction, is to be suspected 
in painful injuries about the shoulder. 

Sprains of the wrist also are probably quite rare, and 
should be diagnosed only when other lesions have been ruled 


118 


INFLAMMATION IN BONES AND JOINTS 


out. In this connection three things especially must be 
borne in mind: 1st, Fractures of the radius or of the 
carpal bones. The Rontgen rays will detect these. 2nd, 
Ganglion. This is a rather small, tense, fluctuating swell¬ 
ing found usually on the dorsal aspect of the wrist, slightly 
to the radial side, or less often on the volar aspect in the 
immediate vicinity of the radial.artery. 3rd, The so-called 
tenosynovitis or tenovaginitis crepitans, a slightly painful, 
diffuse swelling, over the posterior and lateral aspect of the 
distal end of the radius. When the patient actively extends 
and abducts his thumb, a fine crepitation like the rubbing 
together of two j)ieces of silk, is communicated to the 
examining finger. Circular strapping with adhesive tape, 
about two inches wide is a good treatment for a 
sprained wrist. 

Sprains of the spine, especially of the spine already 
affected with a chronic arthritis, are quite common, though 
on account of the inaccessibility of the spinal joints, the 
diagnosis is never more than presumptive. Following a 
severe wrench, twist, or sudden strain, the patient ex¬ 
periences a sudden pain, usually in his lumbar region 
(“lumbago”) or down his thigh (“sciatica”). The pain 
often is quite severe, and as a rule is accompanied by 
marked stiffness of the spine. Sometimes the patient is 
unable to bend forward at all, at other times forward 
bending is carried out with a lateral deviation. When the 
sacroiliac joint is involved, perhaps also when the lower 
lumbar spine is sprained, a Kernig sign is present. An 
Ely sign 2 occasionally may be elicited in lumbar arthritis 
or sprain. 

2 In certain irritative lesions of the lower lumbar spine, if the patient 
lie prone, and his knee be flexed, his pelvis will rise from the table. This 
is the Ely sign, and it is probably caused by the pull forward on the rigid 
lumbar spine by the rectus femoris muscle. 



TRAUMATIC ARTHRITIS 


119 


Treatment.— These cases ordinarily are treated with 
“ antirhenniatic ” remedies as “ myositis,” “ fibrositis,” 
“ lumbago ” or “ sciatica.” A Rontgen plate usually will 
show the evidences of a chronic arthritis, and the main 
efforts at treatment should be directed at this. (See the 
chapter on chronic arthritis.) In sacroiliac sprain the 
X-rays often show a subluxation of the pubic symphysis. 
In the simple cases, snug strapping about the sacroiliac 
joints, below the anterior superior spines may be all that is 
necessary. Physical therapy also has its advocates. Some¬ 
times the subluxated pubic joint must be reduced under an 
anaesthetic. Superextension of the thigh on the affected 
side will usually be found the best manipulation. 


CHAPTER IX 


SUPPURATIVE ARTHRITIS FROM WOUNDS 

The joint may be involved directly by the penetration 
of dirty foreign bodies, or it may be involved secondarily 
by the spread of an infection from a compound fracture 
opening into the joint. In the first case the marrow may 
become infected secondarily from the joint. The infection 
is of course always a mixed one. At its start it possesses 
peculiarities depending upon its jilace of origin, and the 
nature of the trauma, but once under way, its course is 
much the same as that of a hematogenous infection. The 
soft parts may become gangrenous at an early stage. 

Our ideas on the treatment of joint wounds have been 
greatly modified during the late war, and, while unanimity 
has by no means been reached, a fairly well-recognized 
standard of procedure lias been adopted. This may be 
stated briefly as follows: 

In the absence of any sign of infection penetrating joint 
wounds made by sharp instruments, supposedly fairly 
clean, may be treated expectantly with sterile dressings. 
This applies also to perforating wounds made by bullets 
of high velocity, especially in the absence of fracture. They 
must be watched carefully, however, and must be opened 
up at the first sign of an infection. Other wounds 
demand operation. 

The operation of debridement, as practised so ex¬ 
tensively, aims to remove not only the foreign body but 
also its infected track through the tissues. In wounds of 

the soft parts all devitalized tissue in the neighborhood is 
120 


SUPPURATIVE ARTHRITIS FROM WOUNDS 121 

also excised, but this feature is not so prominent in oper¬ 
ations on joints. The wound of entrance is excised down 
into the joint, and the foreign body is removed. If the 
projectile is imbedded in hone or soft tissue, this is removed 
with it. The track of the missile is excised, with chisel and 
gouge, with a curette only if necessary. All foreign bodies, 
such as shreds of clothing, and all loose fragments of bone 
are removed. If the joint has been so badly damaged that 
useful function is not to be expected, resection had best he 
done forthwith. 

After lavage of the j oint cavity with normal salt solu¬ 
tion, the capsule is sutured, and the wound of the skin also, 
unless its infection is suspected. If so, the wound in the 
skin is left open. Some surgeons recommend filling the 
joint cavity two or three times with ether after lavage with 
normal salt solution. If the joint fills with fluid thereafter, 
it should be aspirated. Xo drains should be left in the joint. 
Early active and passive motion, as soon as the wound has 

healed, are very important. 

In this procedure one must always avoid infecting 
sterile tissue. Instruments which have touched infected 
tissue should be discarded for fresh ones, and the gloves 
must be changed as often as necessary. 

In the early stage of infected wounds the same treat¬ 
ment may be earned out tentatively, perhaps modified by 
drainage for a day or two. Uayr maintains that in joint 
wounds without bone damage, the infection is often super¬ 
ficial in the synovial membrane, and can be controlled by 
irrigation (injection), with or without temporary drain¬ 
age, either simply through small openings in the capsule, 
or with a glass tube. 

With frank infections, after thorough debridement 
and cleansing, drainage of course is necessary. Willems 


122 INFLAMMATION IN BONES AND JOINTS 

advises, in addition to the openings in the capsule, 
early active motion to accomplish drainage. Opinions 
differ as to the efficacy of this treatment. The Carrel- 
Dakin treatment has its advocates. Whatever method 
of drainage be adopted, care must be taken that it 
is thorough. It is not enough simply to make openings in 
the joint unless they actually drain it. If necessary, bone 
must be removed, and no recess must be left for the accumu¬ 
lation of pus. Some surgeons advise resection, others have 
been disappointed with the results of the operation. 
Amputation often will be necessary. 


CHAPTER X 


HAEMOPHILIAC JOINTS 

Hemorrhage into the joint, especially into the knee, 
is a fairly frequent occurrence in that interesting condition 
known as the hemorrhagic diathesis or haemophilia. It is 
observed much more often in men than in women, as is the 
diathesis to which it is due. The tendency to bleed un¬ 
controllably at the slightest scratch is hereditary, and is 
handed down through the female element. Addis 1 in¬ 
vestigated a number of these families of “ bleeders ” and 
has added much to our knowledge of the subject of 
haemophilia. It is important to know the manifestations of 
the diathesis in the joints in order to avoid making a blun¬ 
der that may be fatal. 

As the result of a slight trauma, or, as some claim, with¬ 
out trauma, a joint of a bleeder, usually the knee joint, 
swells up, “like a balloon,” as one patient put it. Pain as a 
rule is not a prominent symptom; the chief complaint is the 
interference with function from the presence of the fluid. 
Fluid can be detected in the joint, and sometimes a soft 

1 Addis, T.: “The effect of the adminstration of calcium salts and of 

citric acid on the calcium content and coagulation time of the blood. 

Quart. J. Med. 1908-09, v, 2. 

Addis, T.: “Coagulation time of the blood/’ Brit. M. J., 1909, i, 1151. 

Addis, T.: “The coagulation time of the blood in man.” Quart. J. M., 

1908-09, ii, 305. 

Addis, T.: “The coagulation time of the blood.” Brit. M. J., 1909, i, 1269. 

Addis, T.: “ The coagulation time of the blood in disease.” Edin. M. J., 1910, 
n. s. v. 5. 

Addis, T.: “Hereditary haemophilia; deficiency in the coagulability of the 
blood the only immediate cause of the condition. ’ Quart. J. Med., 1910, v, 4:14. 

Addis, T.: “The pathogenesis of hereditary haemophilia.” J. Path, and 

Bacterial, 1910-11, v, 15:427. 


123 





124 INFLAMMATION IN BONES AND JOINTS 

crepitation. The synovial membrane proliferates, some¬ 
times enormously, and its internal surface may become 



Fig. 40. —Haemarthrosis of the knee in a "bleeder. ” 


shaggy, with the enlarged villi branching like moss 
on a rock. 

The fluid may slowly be absorbed and the joint may 
return to normal, to be again attacked at a later period. 








HAEMOPHILIAC JOINTS 


125 


Again layers of fibrin may be deposited upon the synovial 
membrane and possibly upon the cartilage. These layers 
of fibrin may become organized, and may give rise to dense 
adhesions, which cause a practically complete ankylosis. 

A sudden, fluctuating, comparatively painless swelling 
of a joint without history of injury, in the absence of 
physical signs of tabes, should always awaken the suspicion 
of haemarthrosis, and should occasion a search for a family 



Fig. 4 i_—Skiagram of a case of old fibrous ankylosis in a “bleeder.” 

history of bleeders, and for a personal history of profuse 

hemorrhage after slight injury. 

For the treatment of the acute attack, rest, pressure 
and cold applications are probably best. After the hem¬ 
orrhage has ceased and a little time has elapsed, hot appli¬ 
cations and gentle massage may possibly promote the 
absorption of the exudate. In case of need, blood trans¬ 
fusion may be done, or blood plasma may be injected . 2 
The advantage of any such procedure is temporary only; 

2 Personal note of Dr. Addis: “Hot applications and gentle massage I 
should be afraid to use. I should prefer temporary immobilization with 

pressure. 

“ Blood transfusion should only be used in case of danger to life. This 
would not arise in a hemorrhage confined to the joints. 








126 


INFLAMMATION IN BONES AND JOINTS 


the coagulation time is shortened, but later is lengthened 
again, so that the patient is in greater danger than he 
was before. 

It is hardly necessary to emphasize the importance of 
avoiding in all circumstances and in every stage, any oper¬ 
ative interference with a joint hemorrhage in a bleeder. 

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ACUTE SUPPURATIVE OSTEOMYELITIS 

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Clopton, Malvern B.: “ The diagnosis and treatment of osteomyelitis.” Surg . 
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Dumont, Fritz L.: “ Experimentelle Beitrage zur Pathogenese der akuten 
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116. 

Estor, E., and Etienne, E.: “La greffe graisseuse dans Toblit^ration des 
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Evans, Arthur J.: “Excision of the diaphysis of the humerus with full 
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Fraenkel, Eug. : “ Ueber Knochenmark und Infektionskrankheiten.” Miinch. 
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Gross, Heinrich : “ Zur Kenntnis des osteomyelitischen Knochenabscesses der 
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chen Verhaltens.” Beitr. z. klin. Chir., 1901, xxx, 231. 

Hamant, A., and Pigache, R.: “Osteomyelite a infections mixtes” Gazz. 
d. Hop., 1913, lxxxvi, 1158. 

Hamilton, Frank A.: “Osteomyelitis with bone transplantation.” J. A. M. A., 
1913, lx, 2030. 

Homans, John-: “Osteomyelitis of the long bones,” Ann, Surg., 1912. lv, 375. 
Kennedy, Charles M.: “Acute epiphysitis.” Brit. Med. Jour., 1912, ii, 114. 
Kirmisson: “ Les osteomyelites.” Progres Med,, 1913, xli, 643. 

Klemm, Paul: “Die akute und chronische infektiose Osteomvelitis des 
Kindesalters.” Berlin, S. Karger, 1914. 

Klemm, Paul: “ Ueber die chronische Form der sklerosierenden Osteomyelitis 
des Kindesalters.” Berlin, S. Karger, 1914. 

Klemm, Paul: “ Ueber die chronische Form der skelerosierenden Osteomyelitis 
und ihrer Varianten.” Beitr. z. klin. Chir., 1912, lxxx, 54. 

Klemm, Paul: “Ueber die Gelenkosteomyelitis, speciell die osteomyelitische 
Coxitis.” Arch. f. klin. Chir ., 1912, xcvii, 414. 


HAEMOPHILIAC JOINTS 127 

Klemm, Paul: “ Ueber die Veranderungen der knochernen Grundsubstanz 
bei Osteomyelitis und ihre Ursachen.” Deutsche Ztschr. f. Chir., 1913, 
cxxiv, 309. 

Kocher, Theodor: “Die akute Osteomyelitis. . .” Ztschr. f. Chir., 1878-79, 
xi, 87. 

Lannelongue : “ Des portes d entree de 1 osteomyelite. Soc. de Chir. Bull, 
et mem,., 1886, xii, 474. 

Lannelongue, et Achard: “Des osteomyelites a streptocoques.” Soc. de 
biol. Mem., 1890, 9 ser., ii, 298. 

Lannelongue, et Achard: “Etude experimental des osteomyelitis a 
staphylocoques et a streptocoques.” Ann. de VInst. Pasteur., 1891, v, 209. 
Le Conte! Robert G.: “ Acute inflammation of long bones, with special reference 
to excision of the diaphysis.” Boston Med. Surg., Jour., 1911, clxiv, 771. 
Le Conte, Robert G.: “Acute inflammation of the long bones/’ Ann. Surg., 
1912, lvi, 150 

McGuire, R. Clark : “ Aberrant and recurrent osteomyelitis.” Brit. Med. 
Jour., 1913, i, 13. 

Neuber, G.: “Zur Behandlung starrwandiger Hohlenwunden.” Arch. f. khn. 

Chir., 1896, li, 683. „ 

Nichols, Edward H.: “Acute, subacute and chronic infectious osteomyelitis. 

J. A. M. A., 1904, xlii, 439. 

Park, Roswell: “Acute infectious processes in bone.” Boston Med. Surg., 
Jour., 1895, cxxxii, 425. 

Phelip, J. A.: “ L’osteomyelite des os longs chez lenfant et b adolescent. 
These de Paris, 1912. 

Phemister, D. B.: “ Subperiosteal resection in osteomyelitis.” J. A. M. A., 1915, 
lx.v 1994** 

Phemister, D. B.: “Osteomyelitis.” D. Appleton & Co., New York & London, 
1922. 

Pringle, Seton: “Radical operation for chronic osteomyelitis.” Brit. Jour. 
Surg.. 1913-14, i, 625. 

Rost, Franz: “ Experimented und klinische Untersuchungen liber chron.sche, 
granulierende Entziindungen des Knochenmarks ” Deutsche Ztschr. f. 
Chir., 1913, cxxv, 83. 

Simmons, Channing C.: “Localized osteomyelitis of the long bones. Boston 
Med. Surg., Jour., 1913, clxviii, 637. 

Simmons, Channing C.: “The treatment of osteomyelitis.” Surg., Gynec. 

Obst., 1915, xx, 129. . „ _ . 1Q19 

Strong, G. R.: “Eight cases of osteomyelitis of the spine. Lancet, 191 

ii, 1576. ^ .... , 

Then del: “ Beitrage zur Kenntnis der akuten infectiosen Osteomyel.tis und 

ihrer Folgeerscheinungen.” Bellr. z. klin. Chir., 1904, xli, 607. ^ 

Williams, Gwynne: “The localization of osteomyelitis, especially in adults. 

Brit. J. Surg., 1914-15, ii, 97. , ... „ 

Churchman, John W.: “ Gentian violet in the treatment of purulent arthritis. 

Jour. A. M. A., 1920, lxxv, 583. 


128 


INFLAMMATION IN BONES AND JOINTS 

ACUTE GONOCOCCIC ARTHRITIS 

Corbus, B. C.: “Gonorrheal arthritis.” Medical Clinics of Chicago, 1917, 
ii, 1189. 

Culver, Harry: “Antibodies in gonococcal arthritis after the intravenous 
injection of specific and non-specific protein.” Jour. Lab. and Clin. Med., 
1917, iii, 11. 

Dufour, M. H.: “ Gaillard et Ravina: Sur les lesions des extremites osseuses 
articulaires dans la polyarthrite gonococcique.” Bui. et Mem. d. 1. Soc. 
Med. des hopitaux de Paris, 1919, xxxv, 918. 

Harm'orth, H. D.: “ The treatment of gonococcal arthritis by sensitized 
gonococcal vaccine.” Brit. Med. Jour., 1918, i, 4. 

Malletrre Felix: “Antimeningococcic serum in the joint manifestations of 
gonorrhea.” New York Med. Jour., 1906, ciii, 1024. 

Rogers, John: “The treatment of gonorrheal rheumatism by an antigonococcus 
serum.” J. A. M. A., 1906, xivi, 263. 

Rogers, John, and Torrey, John C.: “The treatment of gonorrheal infections 
by a specific antiserum.” J. A. M. A., 1907, xlix, 918. 

Stockman, Ralph: “The vaccine treatment of gonococcal arthritis.” Brit. 
Med. Jour., 1911, ii, 1465. 

Torrey, John C.: “An antigonococcus serum effective in the treatment of 
gonorrheal rheumatism.” J. A. M. A., 1906, xivi, 261. 

TYPHOID SPINE 

Allan, W., and Squires, J. W.: “Typhoid vaccine in a case of typhoid spine.” 
Amer. Jour. Med. Sciences, 1918, clvi, 11. 

Garnett, J. B.: “Typhoid spine.” Annals of Surgery, 1915, lxi, 456. 

Conklin, C. B.: “Typhoid spine.” Med. Record, 1914, lxxxv, 157. 

Ely, Leonard W.: “A case of typhoid spine.” Med. Record, 1902, Ixii, 966; 
1904, lxv, 655. 

Galli, G.: “Ueber spondylitis typhosa.” Muencli. med. Woch., 1915, lxii, 501. 

Lord, Frederick T.: “Analysis of 26 cases of typhoid spine.” Boston Med. 
and Surg., Jour., 1902, cxlvi, 689. 

Osler, Wm.: “Typhoid spine.” Canadian Med. Ass. Jour., 1919, ix, 490. 

Rugh, J. T.: “Report of a case of typhoid spine.” Am. Jour. Orthop. Surg., 
1915, xiii, 287. 

Rogers, Mark H.: “Pathology of typhoid spine.” Boston Med. and Surg., 
Jour., 1913, clxviii, 348. 

Silver, David: “Typhoid spine.” Amer. J. Orthop. Surg., 1907-8, v, 194, 
(bibliography). 

ACUTE INFLAMMATORY RHEUMATISM 

Fantus, Bernard, Simmonds, Walter E., and Moore, Josiah J.: “The 
effect of salicylates on experimental arthritis in rabbits.” Arch. Int. Med., 
1917, xix, 529. 

Lippmann: “Bacteriologie du rhumatisme articulaire aigu.” Semaine Med., 
1900, xx, 77. 


HAEMOPHILIAC JOINTS 129 

Poynton, F. J., Agasslz, C. D. S., and Taylor, J.: “A contribution to the 
study of the rheumatic infection.” Practitioner, 1914, xciii, 445. 

Poynton, F. J., and Paine, Alexander: Researches on rheumatism. London, 
J. & A. Churchill, 1913. 

Rolly, Fr. : “ 7air Aetiologie des akuten Gelenkrheumatismus.” Med. Klinik, 
1916, xii, 1167. 

Rosenow, Edward C.: “Elective localization of streptococci.” J. A. M. A., 
1915, lxv, 1687. 

Swift, H. F., and Kinsella, R. A.: Bacteriologic studies in acute rheumatic 
fever.” Arch. Int. Med., 1917, xix, 381. 

Weintraud, W.: “ Der acute Gelenkrheumatismus: Spezielle Pathologie und 
Therapic innerer Krankheiten.” Urban u. Schwartzenberg, Berlin, 1913. 

INTERMITTENT SYNOVITIS 

Brackett, E. G., and Cotton, F. J.: “Intermittent hydrops.” Boston Med. 
Surg., Jour., 1901, cxlv, 484. 

Laurie, A.: “ L’Hydarthrose du genou et son traitement cliez les blesses de 
guerre.” Jour, de med, des Bordeaux, 1918, lxxxix, 158. 

Linberger, A.: “ Ueber intermittierenden Gelenkhydrops.” Beitr. z. klin. 
Chir., 1901, xxx, 299. 

MacLf.lland, R.: “Intermittent hydrops articulorum.” Lancet, 1919, i, 463. 
Seelingmuller, A.: “Hydrops articulorum intermittens.” Deutsche med. 
Wchnschr., 1880, vi, 52. 

Tavernier: “ Hydarthroses recidivantes du genou par coincements anatomi- 
ques.” Lyon Med., 1918, cxxvii, 433. 

SUPPURATIVE ARTHRITIS FROM WOUNDS 

i 

Bristow, W. Rowley: “Treatment of joint and muscle injuries.” London, 
Oxford University Press, 1917. 

Burckiiardt, Hans ltnd Landois, Felix: Erfahrungen uber die Behandlung 
inficierter Gelenke im Kriege. “Beitr. z klin. Chir., 1915-16, xcviii, 358. 
Cook, Frank: “Gunshot wounds of joints, their pathology and treatment.” 
Lancet, 1917, i, 711. 

Denk, W.: “Ueber Schussverletzungen der grossen Gelenke.” Beitr. z. klin. 
Chir., 1914, xci, 394. 

Eisendrath, Daniel N.: “Injuries of the joints in war and in civil life.” 
Surg., Clin. Chicago, 1919, iii, 497. 

Jones, Robert: “Injuries to the joints.” London, Oxford University Press, 
1915. 

Murphy, John B.: “Contribution to the surgery of bones, joints and tendons.” 
J. A. M. A., 1912, lviii, 1254. 

Osgood, Robert B.: “Gunshot injuries to the joints.” Jour. Orth. Surg., 
1919, i, 304. 

Payr: “Arm-und Beinschussbriicke; Gelenkschusse; Gelenkeiterungen. Beitr. 
z. klin, Chir., 1915, xcvi, 529. 


9 


130 INFLAMMATION IN BONES AND JOINTS 

Payr: “ Gelenkverletzungen, Gelenkeiterungen und ihre Behandlung.” Munch, 
med. Wchnschr., 1915, lxii, 1321. 

Payr: “Gelenkverletzungen, Gelenkeiterungen und ihre Behandlung.” Miinch. 
med. Wclinsclir., 1915, lxii, 1282. 

Payr: “Gelenkverletzungen, Gelenkeiterungen und ihre Behandlung.” Miinch. 
med. Wclinsclir., 1915, lxii, 1241. 

Pool, Eugene: “War wounds.” J. A. M. A., 1919, lxxiii, 383. 

Pool, Eugene H., and Jopson, John H.: “Treatment of recent wounds of 
the knee-joint.” Ann. Surg., 1919, lxx, 266. 

Pool, E. H., Lee, B. J., and Dineen, P. A.: “Surgery of soft parts, bones, 
and joints, at a front hospital.” Surg., Gynec. Obst., 1918, xxvii, 289. 

Swan, Jocelyn R. H.: “Severe infected gunshot injuries of the shoulder and 
elbow joints; early excision to secure mobility.” Lancet, 1917, i, 524. 

Willems, Ch.: “ Quelques resultats du traitement des lesions articulaires par 
la m^thode de la mobilisation active immediate.” Soc. d. Chir. Bull, et 
Mtm., 1917, xliii, 1784. 

HAEMOPHILIAC JOINTS 

Cruet, Pierre: “ Hemophilie articulaire.” Presse Med., 1906, xvi, 578. 

Deribere-Desgardes, Pierre: “Des arthropathies chez les hemophiles.” Th&se 
de Paris, 1910. 

Escande, F., and Tapie, J.: “ Sur un cas d’hemophilie articulaire.” Jour, de 
radio!, et d’6lec., 1919, iii, 298. 

Gayet, M. G.: “Arthropathies et hematomes diffus chez les hemophiles.” Gaz. 
Lebd. de Med. et. de Chir., 1895, xxxii, 258. 

Gocht, Hermann: “ Ueber Blutergelenke und ihre Behandlung.” Arch. f. 
Klin. Chir., 1899, lix, 481. 

Konig, Franz: “Die Gelenkerkrankungen bei Blutern mit besonderer Ber- 
iicksichtigung der Diagnose.” Samml. Jclin. Vortr. Chir., 1890-94, v, 233. 

Leclerc, F., and Chalier, J.: “Hemophilie familiale.” Lyon Med., 1912, 
cxix, 589. 

Mankiewicz: “Ueber Blutergelenke.” Berl. klin. Wchnschr., 1913, 1, 2174. 

Martin-Du Pan, Charles: “ De l’arthropathie hemopliilique.” Rev. Med. de 
la Suisse Rom., 1915, xxxv, 547. 

Mery, H., Salin, H., and Wilborts, A.: “Deux cas d’hemophilie familiale. 
Arthrite hemopliilique simulant 1’ osteomyelite.” Soc. de pediat. de Paris, 
Bull., 1913, xv, 86. 

Piollet, M. P.: “Les arthropathies hemophiliques.” Gaz. d, hop., 1902. 
lxxv, 385. 

Roth, Paul B.: “ Case of haemophilia with effusion into knee-joints.” Brit. Jour., 
Child. Dis., 1918, xv, 116. 

Well, P. E., and Boye : “ Hemophilies humaine animale et experimentale,” 
Cong. Internat. de Path. Comp., 1912, ii, 335. 

Youmans, John B.: “Report of case of hemophilia with joint involvement” 
Wis. Med. Jour., 1919-20, xviii, 257. 


SECTION III. 


CHRONIC OSTEOMYELITIS 



CHAPTER I 


PHOSPHORUS NECROSIS 

Indirectly, and consequent upon the changes in the 
bone produced by phosphorus, bacteria from the mouth 
may cause a chronic suppurative osteomyelitis in the maxilla 
or more often in the mandible. The disease is usually found 
in workers in phosphorus match factories, and especially 
among those who have bad teeth. With the introduction of 
sanitary precautions it has grown rare. 

Hand in hand with the suppuration and necrosis in the 
bone and in the marrow, goes the production of new bone 
not only in the periosteum, but sometimes in the bone itself. 
The teeth loosen and fall out, and the soft tissues become 
infiltrated and inflamed. The entire mandible may be killed, 
and its articulation may become ankylosed. Death often 
results. After the removal of the mandible a new bone may 
be formed by bone production in the periosteum. 

The treatment is prophylactic and operative. The 
mouth and teeth of match-makers should be kept scrupu¬ 
lously clean and in good condition. Factory employes 
should not eat nor drink in their work-rooms, and by atten¬ 
tion to their hands and to their finger nails should avoid 
carrying any phosphorus into their mouths. Work-rooms 
must be kept clean and well-ventilated. Where proper 
precautions are observed, phosphorus necrosis will rarely 
be seen. 

The operative treatment consists in the resection of the 
diseased bone. The resection should be a free one, and all 
the affected tissue must be removed. As a rule new bone 
will be built up to replace that which is removed. 


133 


134 


INFLAMMATION IN BONES AND JOINTS 
SCLEROSING OSTEOMYELITIS 


A rather rare form of osteomyelitis, the so-called scleros¬ 
ing osteomyelitis, has been described which has an acute or 
subacute onset and does not lead to the immediate formation 
of pus. More or less of the bone becomes very dense and 
thickened. Sometimes small abscesses with sequestra are 
found in this mass of dense bone. Whether this disease 
should be included under the head of acute or of chronic 
osteomyelitis is doubtful. The treatment consists of eradi- 
eating any 2)ossible focus of infection in the body, and 
cleaning out any abscesses with the surrounding scler¬ 
osed bone. 

Another rather bland form of chronic osteomyelitis is 
occasionally seen in workers in mother-of-pearl. It has no 
tendency to suppurate, and yields readily to the removal of 
its cause. 


CHAPTER II 

SYPHILIS 


The bone manifestations of syphilis are very frequent. 
Not only is the infection carried to the bone marrow at an 
early period, hut it remains there almost indefinitely. It 
manifests itself in the secondary and in the tertiary stages, 
and also after the subsidence of the active period of the 
disease in the form of the so-called “neurotrophic” 

bone lesions. . 

Congenital bone syphilis is fairly frequent, m fact its 

lesions are among the most characteristic in the boch. 
lias been pointed out that congenital syphilis is really 
acquired syphilis, acquired in utero, and that its peculi¬ 
arities are due simply to the differences in foetal and 
infantile tissues from those of the adult. Hereditary 
syphilis probably is a misnomer, as implying an infection o 

the germ plasm. . 

In studying syphilis of the bones and joints one is struck 

by the marked, and, at first sight, unaccountable difference 
of opinion that prevails on most phases of the subject, u 
the difference of opinion is not so strange as it seems. I ntil 
the last few years the cause of syphilis had not been ic enti- 
fied. Therefore the diagnosis rested upon the lnstoiy, 
upon the presence of other known (or presumptive) evi¬ 
dences of syphilis, upon the therapeutic test, or upon ail 
three. Even to-day the vast majority of clinical diagnoses 
is made without the demonstration of the spirocheta pa i- 
dum, and in such cases the pathologist never receives any 
of the material for examination, for no operation is done. 

135 


136 


INFLAMMATION IN BONES AND JOINTS 


On the other hand the pathologist regularly performs 
necropsies upon the bodies of still-born foetuses and of 
young infants, in which he can demonstrate syphilis. With 
these cases the clinician is not brought into contact. The 
morbid processes observed by the pathologist and by the 
clinician appear to be entirely different, but in point of fact 
they are quite the same, and differ only in location 
and details. 

Pathology.— The characteristic lesion of syphilis in 
bone is a proliferative inflammation in the marrow—a 
syphiloma, a gumma. This may occur in any part of the 
bone, though its situation is largely determined by the age 
of the patient. In congenital syphilis, as seen in infants 
and children, the ends of the long bones and the shaft of the 
bones of the hands suffer most; in the adult the shaft of the 
long bones is most often attacked. The resulting process 
depends largely upon the location. While certain peculiar 
types of osseous syphilis can be recognized as more or less 
standard, it is necessary to remember that they are by no 
means invariable, and that here as elsewhere in the body, 
the disease often manifests itself in most unusual ways. 

EARLY CONGENITAL SYPHILIS 

Although a few cases of congenital bone syphilis had 
been published, the disease was considered to be very rare, 
in infants and children, until the publication of Wegner’s 
article in 1870. 1 Then quickly the investigations of 
Parrot 2 and of Waldeyer and Koebner, 3 in 1872, and of 

1 Wegner, George: “ Ueber heredidaere Knochensyphilis bei jungen 
Kindern.” Archiv. f. Path. Anat. w. f. klin. Med,, 1870, i, 305. 

2 Parrot, M. J.: “ Sur une psendo-paralyse . . . de syphilis hereditaire.” 
Archives, d. Physiol. Normale e. Path., 1872, iv, 319, 470, 612. 

3 Waldeyer u. Koebner: “ Beitraege zur Kenntnis der hereditaeren 
Knochensyphilis.” Arch. f. Path. Anat. 1872, Iv, 367. 





SYPHILIS 


137 


Taylor, 4 in 1874, established the fact that bone lesions in 
early congenital syphilis, so far from being infrequent, 
were among the most common manifestations of the disease. 

The peculiar lesion of congenital syphilis, the “ osteo¬ 
chondritis syphilitica ” of Parrot is located immediately 
adjacent to the epiphysial cartilage on its shaft side, that 
is, in and near the zone of provisional calcification. It con¬ 
sists essentially in a syphilitic myelitis. The new granula¬ 
tion tissue in the marrow breaks up the regular formation 
of hone. Under the microscope one sees tongues of it 
pushing up into the epiphysial cartilage. The columns of 
calcified and calcifying cartilage matrix in the zone of pro¬ 
visional calcification are, to a great extent, absorbed, so 
that the zone or a part of it may eventually consist of little 
else than granulation tissue, separating the epiphysis 
partially or completely from the shaft. Later the granu¬ 
lation tissue undergoes necrosis. 

The zone of provisional calcification becomes much 
wider than normal and appears as a fairly broad white or 
pinkish band, irregular in its outline, instead of as a thin, 
barely perceptible line. Later the tissue breaks down and 
becomes a mass of grayish-white, brittle, mortar-like 
material, either in a small area or running across the entire 
width of the bone and possibly separating the epiphysis 
from the shaft. The process in the marrow is not regular 
and sharply defined, but decidedly irregular, wavy, and 
notched. Vessels from the marrow push up into the 
epiphysial cartilage. The resulting irregular outline of 
the shaft side of the epiphysial cartilage, somewhat similar 
to that in rickets, is perceptible to the naked eye and 
appears also in the X-ray plate. The X-ray shows also a 

4 Taylor. R. W.: “Syphilitic lesions of the osseous system in infants and 
young children, etc.” Am. J. Obstet., 1874, vii, 53, 177, 559. 




138 


INFLAMMATION IN BONES AND JOINTS 


rarefaction of the bone corresponding to the irregular area 
of the disease, on the shaft side of the epiphysial cartilage. 
The broken down syphilitic granuloma may later break 
through the periosteum and communicate with the surface 
and become secondarily infected, or resolution may take 
place under appropriate treatment. If the epiphysis have 
been separated, union usually is brought about by new bone 
laid down in and under the periosteum, and the growth of 
the limb is not retarded. 

The changes described above are often seen in still-born 
syphilitic foetuses. They may, however, be present in 
syphilitic children born alive or may appear during the first 
few months of life. They occasion swellings in the bone 
in the neighborhood of the joint, sometimes quite painful 
and sensitive to pressure, sometimes not so painful. The 
resulting condition is what Parrot described as “ pseudo¬ 
paralysis.” The limb hangs limply. The child refuses to 
move it, and cries when it is moved. With separation of 
the epiphysis, a false point of motion can be found, with a 
soft crepitus. When union has been brought about, the 
thickened periosteal bone, shaftward from the epiphysis 
can be felt. 

The gross changes in and about the epiphysis are some¬ 
what similar to those seen in rickets, and the similarity is 
so great that certain observers in the past have thought that 
syphilis was the cause of rickets. The essential points in 
the diagnosis are: first, syphilis appears at an earlier age 
than rickets; second, with syphilis other marks of the dis¬ 
ease such as roseola, mucous patches, etc., are usually 
present, possibly also other changes in the shafts of the 
long bones and the skull; third, the changes about the 
epiphysis in syphilis usually, as far as clinical evidence 
goes, are single or at best are evident in only two or three 


SYPHILIS 


139 


places, whereas with rickets they are more or less general; 
fourth, syphilis is more painful than rickets. 

The changes in the region of the epiphysis in scurvy, are 
somewhat similar clinically to those of syphilis, hut scurvy 
usually appears somewhat later, the irregular appearance 
of the zone of calcification and the bone absorption do not 
appear in the X-ray plate in scurvy, the onset is sudden, 
the pain perhaps is more severe, other signs of syphilis are 
absent, and signs of scurvy, such as hemorrhages from the 
gums are present. 

Besides this so-called syphilitic osteochondritis another 
notable marrow change is often met with in young syphilitic 
children according to Wegner, namely fatty degeneration 
of the vessels and cells of the marrow. This may be more 
or less diffuse, or may he circumscribed, and gives to the 
hone marrow a yellowish or pinkish yellow color. Perhaps 
to these extensive marrow changes is due the well known 
a mem i a of syphilitic children. 

In older children three syphilitic lesions are often found 
in the hones of the extremities: first, cortical changes 
similar to those of the adult, later to be described; second, 
disease of the bones of the hand, most often of the proximal 
phalanx, similar to the spina ventosa of tuberculosis; third, 
disease of the ends of the long bones with an accompany¬ 
ing arthritis. 

Syphilitic disease of the marrow of the hones of the 
hand is fairly frequent in children. It causes a rarefaction 
of the bone and an enlargement, more or less general, but 
especially marked at its proximal extremity. It shows 
little or no tendency to involve the joint, and quite often 
breaks through the cortex and the periosteum, communi¬ 
cates with the surface, becomes secondarily infected, and 
leads to the establishment of persistent sinuses. The 


140 


INFLAMMATION IN BONES AND JOINTS 


irritation of the disease in the marrow with the resulting 
destruction of bone in the interior, is said to cause the 
formation of new bone in the periosteum, perforated in one 
or more places for the discharge of the necrotic material 
within. A probe passed through one of these holes in the 
shell of the bone easily enters the large cavity. 

This syphilitic dactylitis is as a rule not very painful. 
The swelling may be slight but usually is quite well 
marked, giving the bone twice or thrice its normal diam¬ 
eter. The length of the bone may also be slightly increased. 



Fig. 42.—Dactylitis, probably syphilitic but treated for a long time 

as tuberculosis. 


The general shape of the bone in its breadth is round, while 
it appears to have in its longitudinal direction an oval 
shape (Taylor). It is somewhat broader at its base than 
at its distal end, and the swelling begins quite perceptibly 
at the metacarpo-phalangeal joint, which it enlarges, and 
ends somewhat abruptly at the next joint, that is, of course, 
with disease of the proximal phalanx, the usual lesion. The 
integument is usually stretched and may or may not 
be reddened. 

The Rontgen rays show the irregular structure of the 
bone, and its enlargement, especially at the proximal end. 
This peculiar shape of the bone may help in the differentia- 




SYPHILIS 


141 


tion of syphilitic from tuberculous dactylitis, as may the 
presence of other syphilitic lesions in the body, and perhaps 
the reaction to anti-syphilitic treatment, but very often the 
problem cannot be solved without the aid of the microscope 
and the guinea-pig test. 

With syphilitic involvement of the marrow in the ends of 
the long bones in children a pathological process results in 
the bone and joint so similar to that of tuberculosis that the 
clinical differentiation may be extremely difficult or even 
impossible. Not only are the essentials of the pathological 
process the same, but also the symptomatology and physi¬ 
cal signs. The realization of this fact alone will save one 
from humiliating mistakes. The differential diagnosis will 
be taken up under the head of tuberculosis. 

One of the best known evidences of congenital syphilis 
in the child is the so-called “ saber shin,” an anterior 
bowing of the tibia probably caused by a chronic syphilitic 
process in the marrow in the superficial part of the cortex. 
It gives to the child’s legs a characteristic appearance, not 
to be forgotten when once seen, and hardly to be confused 
with the outward bend of the ordinary bowlegs. 

BONE SYPHILIS IN THE ADULT 

Syphilitic osteomyelitis is frequent in the adult. 
The gummatous inflammation causes primarily, whatever 
its situation, a rarefaction, an absorption of the bone, and, 
if the process be very severe, death of the bone to a greater 
or less extent. The tissue breaks down and forms jelly- 
like or mucilaginous or cheesy masses, which may be 
absorbed under appropriate treatment, may be encapsu¬ 
lated, or may become secondarily infected and lead to the 
formation of sinuses. 

Probably this syphilitic inflammation can exist in any 


142 


INFLAMMATION IN BONES AND JOINTS 


part of the bone marrow, but it occurs in an overwhelming 
proportion in the superficial part of the cortex directly 
under the periosteum. The bone becomes spongy and later 
sclerosed in that locality, and new bone is produced in 
and under the periosteum. This new bone production 
dominates the clinical picture and gives the entire lesion its 
stamp, and it is customary to allude to this form of syphilis 
as a periostitis, and to regard bone production as the essen¬ 
tial factor. The great weight of authority is in favor of this 
view, but I believe it is an error, and consider the sequence 
to be: first, proliferative inflammation in the marrow; 
second, bone destruction; and third, bone formation. This 
so-called syphilitic periostitis probably may occur almost 
anywhere in the body, but its favorite location in the ex¬ 
tremities, is in the shafts of the long bones, especially in 
that of the tibia. It may appear in the form of a more or 
less circumscribed swelling, or in a more diffuse and irregu¬ 
lar thickening of the entire shaft or of a portion of it. 
Again the new periosteal bone may be present in 
small patches. 

This cortical lesion possibly may occur in any period of 
congenital syphilis, but is considered more or less charac¬ 
teristic of the tertiary stages of the acquired form. It may 
be painless or comparatively so. but usually is quite pain¬ 
ful; in fact the boring pains of this form of bone syphilis, 
with their nocturnal aggravation, are notorious. Local sen¬ 
sitiveness is usually present. The overlying tissues may or 
may not be inflamed. If the gumma break down and 
become secondarily infected, a sinus is formed which 
may persist indefinitely, and in a general way may be said 
to resist treatment in proportion to the length of time it 
has existed. The openings of these sinuses are wont to be 
dark red, dirty, sluggish, undermined and ragged, not 
pale, puffy and pouting, like the tuberculosis sinus. 


SYPHILIS 


143 


X-ray Diagnosis. —Syphilis usually involves more 
than one bone; osteomyelitis usually only one bone. 
In syphilis there is rarely the extensive demineralization 
(so-called “ bone atrophy ”) which is a prominent feature 
of osteomyelitis. 

Syphilis involves especially the superficial part of the 
cortex, the only medullary involvement usually being by a 
smooth narrowing of the medullary canal, due to the thick¬ 
ening of the cortex at the expense of the medulla; whereas 
osteomyelitis begins as an acute myelitis with secondary 
periostitis, of a less regular type. 

These points apply to active cases alone. Old lesions 
are frequently impossible to differentiate. 

Bone forming sarcoma of the periosteal type may he so 
characteristic as to be in little danger of confusion. The 
fungoid, “hair on end” appearance (“whiskers”), due to 
the vertically disposed bone “rays” serves to differentiate 
from other proliferations. Bone forming sarcoma pro¬ 
duces enlargement of the bone, which is locally more ex¬ 
tensive than the enlargement of lues or osteomyelitis, but 
which does not extend so far up or down the shaft. Also 
there is much less proliferation in comparison with the 
amount of enlargement. 

It is necessary to say that the X-ray diagnosis is sug¬ 
gestive, not final. I have seen a mixed series of cases 
thrown on the screen whose nature defied detection. 

Syphilitic disease of the marrow of the spongy bone of 
the spine and extremities, is not nearly so frequent as the 
preceding, that is as far as one can judge from clinical 
evidence. It causes a diffuse and more or less irregular 
absorption of the bone, as revealed by the Bontgen rays, 
very like that caused by tuberculosis, and som etimes not to 
be distinguished from it by clinical examination. These 
lesions in the spongy hone do not show a marked tendency 


144 


INFLAMMATION IN BONES AND JOINTS 


to break down, are usually slow and chronic, are often 
painless, and, unlike tuberculosis, may exist indefinitely 
in the immediate neighborhood of the joint without 
involving it. 

The X-ray picture is similar to that of the members of 
the first great type of arthritis, for new bone production 



Fig. 43.—Bone syphilis. The patient of whose radius this is a picture had been treated fora 
long time lor tuberculosis, and recovered under appropriate treatment. 


in the periosteum is not always to be found in the neighbor¬ 
hood of the joint in this form of syphilitic myelitis. The 
diagnosis is made by the history, by the detection of other 
signs of syphilis in the body, especially new periosteal bone 
in othei locations, by the Wassermann and Noguchi re¬ 
actions, and, of greatest importance, by the results of anti- 
syphihtic ti eatment. It is a safe rule to regard every case 
of suspected tuberculosis as possible syphilis until syphilis 
has been definitely ruled out. On the other hand, the rare 








SYPHILIS 


14 


cases of shaft tuberculosis are 
usually mistaken for syphilis. 
Radiologically the two are 
the same. 

A third and much rarer 
form of bone syphilis is a gum¬ 
ma of the central marrow canal. 
This usually results in the 
formation of a more or less 
circumscribed collection of 
mucilaginous material in the 
medulla, about which the bone 
may or may not he sclerosed. 

1 his lesion, as a ride, is not very 

•/ 

painful, but the reaction in the 
periosteum oyer the portion of 
the bone where it is situated 
causes a certain degree of local 
sensitiveness. The Rontgen 
picture may he quite similar to 
that of a bone cyst, hut careful 
observation usually detects new 
hone production in the perios¬ 
teum over the gumma, whereas 
this bone production is absent 
in the ordinary bone cyst. 

Besides the syphilitic ar¬ 
thritis resulting from disease in 
the marrow of the neighboring 
hone, another form of syphilitic 
arthritis is fairly frequent in 
the tertiary stages of the dis- 



Fig. 44. —Syphilis of the shaft of the 
humerus. This case was operated on 
with an erroneous diagnosis of bone 
cyst. Note the reaction in the peri¬ 
osteum, which should have made a 
correct diagnosis easy. 



146 


INFLAMMATION IN BONES AND JOINTS 


ease. It is essentially a proliferative inflammation of the 
synovial membrane—a syphilitic synovitis—and shows 
little or no tendency at any stage to involve the bone 
marrow. The synovial membrane proliferates and becomes 
villous, and pours out a secretion which fills the joint. This 
syphilitic synovitis may be uniarticular or multiarticular, 
affects by preference one or both knees, is usually practi¬ 
cally painless, and responds promptly to treatment. The 
skiagram is negative except for the swelling of the 
soft parts. 

Tabetic joints and bone lesions are an interesting 
manifestation of late syphilis. They are probably degen¬ 
erations rather than inflammations. Whether or not they 
should be included in a book on bone and joint inflamma¬ 
tion, is doubtful. 

Treatment. —This, in its main features, is that of 
syphilitic lesions anywhere in the body, namely by ars- 
phenamin, mercury and the iodides. The restoration of the 
normal structure of an apparently hopelessly damaged 
bone or joint is sometimes remarkable, but when secondary 
infection has taken place the treatment must often be 
continued for a long time. Of course operations should 
be avoided if possible, and this fact is well known. The 
tendency of clean wounds to break down after operations 
on syphilitic bones is also well known. A peculiar fact, 
or possibly a theory, in the treatment of syphilitic 
arthritis is the lack of response to immobilization of the 
joint, and this fact is not without value from a diag¬ 
nostic standpoint. If a syphilitic joint be immobilized, 
pain does not decrease as a rule. Indeed, in contrast to 
tuberculosis, it may grow worse, and necessitate the 
removal of the dressing. 





CHAPTER III 


CHRONIC OSTEOMYELITIS OF UNKNOWN ORIGIN 

Under this heading can be included a number of clini¬ 
cal forms of marrow inflammation whose identity is not 

%/ 

firmly established, and whose differentiation is by no means 
definite or exact. Indeed that they are all marrow inflam¬ 
mations is not universally acknowledged. Three of them 
may be grouped. They possess in common certain patho¬ 
logical features, some of which may be regarded as an 
exaggeration of those ordinarily observed in the bones with 
the advancement of age. They are probably closely 
related, and probably are variations of the same process. 
They are Paget’s disease, or ostitis deformans, leontiasis 
ossea, and the so-called ostitis fibrosa. Even to find a 
name under which to group them is not easy, but for con¬ 
venience, we will call the group 

OSTEOMYELITIS FIBROSA 

The first and probably the fundamental change in the 
members of this group is a fibrosis of the marrow. With 
this goes an irregular production and absorption of bone, 
with or without the formation of osteoid tissue. Cyst 
formation is also a frequent accompaniment. These 
characteristics, as we shall see, are shared by the second 
great type of arthritis, and some writers with good reason 
have regarded the two diseases as essentially variations of 
the same pathological process. Others deny any relation 
between them. 


147 


148 


INFLAMMATION IN BONES AND JOINTS 



Pig. 45.—Paget’s deforming osteomyelitis; 
Stanford Clinic Case No. 1. 


This disease was first 

established as a clinical 

entity by Sir James Paget, 

who, in a paper read before 

the Royal Medical and 
*/ 

Chirurgical Society, placed 
five cases of it on record in 
such detail that little defi¬ 
nite has since been added to 
his description. 1 Five years 
later he published seven 
more cases. 2 The disease is 
comparatively rare, though 
probably not as rare as is 
generally thought. Four or 
five cases are on record at 
Stanford. 

^Etiology. — Nothing 
definite is known as to this. 
The whole appearance of 
bone and marrow is that of 
a low grade chronic infec¬ 
tion, though no definite 
proof of an infection ever 
has been adduced. The 
theory that the disease was a 
manifestation of syphilis has 
been advocated, but has been 


1 Paget, James: “On a form of chronic inflammation of bones.” Medico- 
chirurgical transactions , 1877, lx, 37. 

2 Paget, James: “Additional cases of ostitis deformans.” Med. Chir. 
Trans., 1882, lxv. 225. 


PAGET’S DEFORMING OSTEOMYELITIS, 
OSTITIS DEFORMANS 









CHRONIC OSTEOMYELITIS 149 

\ (liscai (led• Several of Paget’s cases died 

of malignant disease, and Paget thought that there was 

same causal relation between the two, but other observers 

have not confirmed his observation. The similarity of 

« 


Fig. 46. —Paget’s deforming osteomyelitis; Stanford Clinic Case No. 2. 

Paget's disease to the second great type of chronic arthritis 
might suggest the alveolar processes of the jaws as a pos¬ 
sible atrium of infection. 

Paget’s disease is essentially a disease of middle and 
later life, though one case was observed at the age of 






150 


INFLAMMATION IN BONES AND JOINTS 


twenty-one. It is most commonly seen after forty, and the 
majority of patients have been men. A slight familial 
tendency has been noted. 

The bones most frequently and most severely affected 
in Paget’s disease are the tibia, the femur, the calvarium, 



Fig. 47. —Paget’s deforming osteomyelitis. Photograph of one of 
Doctor Ethan Smith’s patients. 

the clavicle, and the spine. Apparently almost all the 
bones of the body may be involved except those of the face, 
which always escape. 

The disease begins in the superficial part of the bone 
cortex. Probably the initial macroscopic change is a rare¬ 
faction of the bone in this vicinity, a rarefaction which 





CHRONIC OSTEOMYELITIS 


151 


slo cL cXiiccs urw i cl. An irregular production of osteoid 
tissue and new bone, especially new periosteal bone, follows 
this, overshadows the initial rarefaction and clinically is by 
far the most prominent feature of the disease. The bones 
become thickened and deformed, and, composed as they are 



Fig. 48.—Paget’s deforming osteomyelitis. Skiagram of the skull 

of poorly formed bone tissue, yield to pressure and to 
strain. The head sinks between the shoulders, the clavicles 
become prominent, the spine bows and sinks together, and 
the femora and the tibias bow outward. The skull may 
become enormously enlarged, sometimes with a smooth 
surface and sometimes with irregular nodules. As the 
result of the shortened trunk and the bowed extremities 
the arms appear disproportionately long. This gives to 





152 


INFLAMMATION IN BONES AND JOINTS 



Fig. -19. I aget a deforming osteomyelitis. -Skiagram of the bones of the legs. 





153 


CHRONIC OSTEOMYELITIS 

the patient an appearance which has been well likened to 
that of an anthropoid ape. 

Histology. —The marrow consists of a vascular con¬ 
nective tissue, more or less rich in cells. Typical giant 
cells are often seen, sometimes in great numbers, and giant 
cell tumors are not rare in this disease. The Haversian 
canals are widened and are filled with vascular tissue, espe¬ 
cially in the superficial portions of the hone. The whole 



Fig. 50. —Paget’s deforming osteomyelitis—Doctor Ethan H. Smith’s second case. This 
photograph was taken in 1906, and the disease then was presumably of about twenty years 
standing. Eight years later the femur was fractured at about the junction of its proximal 
and middle third. The fracture did not unite. Doctor Smith amputated about five months 
later. He “pinched the neck of the femur off” between his thumb and forefinger. The bone 
must have been very soft. The next figure shows the specimen. 

architecture of the bone is changed. The Haversian sys¬ 
tems as such are obliterated, the cortex is thickened and the 
central marrow canals or the diploe may be obliterated by 
the overgrowth of new bone and osteoid tissue. Some¬ 
times the new bone is of normal consistency, sometimes it 
cuts easily with a knife. At times greater or smaller 
islands of sclerosed bone tissue are formed in the midst of 
the other bone. The osteoid tissue evidently may be ossi¬ 
fied later, or at times may itself fall a victim to absorption. 
The margins of the trabecula? often show the classic picture 
of rarefying ostitis—so-called osteoclasts in Howship’s 
lacunas. Cysts have been observed in some cases. In 








154 


INFLAMMATION IN BONES AND JOINTS 



fc.—... 

Fig. 51. Distal two-thirds of femur, and proximal end of tibia of Doctor Smith’s 
second case, sawn sagittally. Note the disorganization of the extreme distal end of 
the femur, and the complete change from the normal architecture of the whole bone. 

The cortex cut easily with the knife, in the laboratory. It consisted of rather open- 
meshed fibrous tissue containing scattered, slender bone trabecuke. 

noticed by the patient is that he is compelled to wear a 
larger hat than formerly, and must increase its size as time 
goes on. When the bones of the lower extremity are first 
involved, then their bowing will he the first thing noticed. 
The X-ray picture will show a marked thickening of the 
affected bones, usually more or less irregular in structure. 
Border line cases may sometimes be hard to distinguish, 
but the typical case of Paget’s deforming osteomyelitis is 
easily recognized. The enlarged cranium, the bowed and 


Paget’s cases “the medullary structures appeared to the 
naked eye as little changed as the periosteum.” 

Strange to say, in spite of all the bone absorption, frac¬ 
tures do not often occur in Paget’s disease. 

Symptomatology. —Pain may or may not be present. 
As a rule it is not severe. Frequently the* first thing 







CHRONIC OSTEOMYELITIS 


1 55 


shortened spine, the bowed lower extremities, the short neck 
and the ape-like build present a picture not easily confused 
with anything else. The disease is probably not as rare 
as has been thought, and escapes recognition only when one 
is not alive to the possibility of its occurrence. 

Treatment. —No treatment has ever been accepted 
for this disease. On the theory that the appearance of 
the marrow indicates a low-grade chronic infection as a 
causal factor, a search should be made for a focus of infec¬ 
tion anywhere in the body, especially in the teeth. If one 
he found, it should be removed. Following out what at 
present is little more than a theory, it will be well to search 
for the amoeba in the intestinal canal. 

LEONTIASIS OSSEA 

The pathological features of this disease are similar to 
those of the preceding. Its distinguishing characteristic, 
however, is a marked involvement of the bones of the face, 
giving to the patient the appearance of one with leprosy. 
It is of very infrequent occurrence. Besides the ordinary 
symptoms of pain and discomfort, the involvement of the 
facial bones may cause severe disturbance in the organs 
of special sense. 

Nothing is known as to the cause of leontiasis ossea, nor 
as to its treatment. On the chance that it may be caused 
by some obscure source of infection, any focus of possible 
infection should be sought and removed, especially in 
the jaws. 

OSTEOMYELITIS FIBROSA, OSTITIS FIBROSA 

Without the peculiarities of the two last named diseases, 
a form of chronic osteomyelitis occasionally is seen, char¬ 
acterized by the change of the marrow to fibrous tissue. 
Giant cells are frequent in this fibrous tissue. The disease 



156 


INFLAMMATION IN BONES AND JOINTS 


may be generalized or local. Cysts may form in the fibrous 
tissue, and the architecture of the bone is usually changed. 
The bone may be distended, but the thickened cortex and 
the periosteal reaction observed in syphilitic disease is 
absent. Pain may or may not be present. Fracture occa¬ 
sionally occurs. The diagnosis is made with the Ront- 
gen rays. 

The cause of this disease also is not known, but it is 
probably some obscure form of infection, possibly in the 
jaws. The tendency of the marrow to become fibrous as 
age advances, is to be borne in mind. 

Treatment. —Any focus of infection should be re¬ 
moved. Cysts may be cleaned out by operation. 

Giant cell growths in bone, the so-called giant cell sar¬ 
comata or benign myelomata are quite similar to the pre¬ 
ceding, are probably inflammatory, and should be classified 
with the chronic inflammation, but as they are usually 
regarded as new growths, they will be omitted from 
consideration. 

PULMONARY HYPERTROPHIC OSTEOARTHROPATHY 

Somewhat akin to the preceding diseases is a rather 
rare condition first described by Bamberger, and later, by 
Marie, whose bone manifestations apparently consist of 
a chronic osteomyelitis with a production of new periosteal 
bone. The name is a most unfortunate one in every re- 
spect,but until we know more about the disease, it is hardly 
worth while to change its name. In the first place, it is 
caused by other things than pulmonary lesions, and in the 
second place the disease apparently may exist without any 
bone or joint involvement whatever. 

^Etiology. —Four groups of causes may be enu¬ 
merated : 



CHRONIC OSTEOMYELITIS 


157 


1. Suppurative or gangrenous processes in the lungs 
or pleura. 

2. Infectious diseases. 

3. Valvular heart lesions, especially congenital. 

4. Malignant tumors in the lung or in the mediastinum. 

Symptomatology. —What has alwavs been considered 

%/ 

the distinguishing mark of the disease is a clubbing of the 
terminal phalanges of the fingers (the Trommelschlegel- 
finger of the Germans), together with a curving or beak¬ 
like deformity of the nails. The fingers are wont to be 
cyanosed as well. The swelling of the end phalanges is 
entirely in the soft parts: The bone is not affected. 

Associated with this peculiar deformity may be a thick¬ 
ening of the rest of the fingers, and sometimes also of the 
forearm (or leg) as well. Examination shows that this 
thickening is due to new bone formation, which is plainly 
shown by the X-rays to be located on the outside of 
the cortex. 

Treatment. —This consists in the removal of the cause 
if possible. Definite improvement has been reported from 
successful treatment of the causal lesion. 

REFERENCES 

HYPERTROPHIC PULMONARY OSTEOARTHROPATHY 

Bamberger, E.: “Ueber Knochenveraenderungen bei chronischen Lungen-und 
Herzkranken.” Zeitsch. f. klin. Med., 1890-91, xviii, 193. 

Janeway, T. C. : “Hypertrophic osteoarthropathy, etc.” Am. J. Med. Sci. 
1903, n. s. cxxvi. 563. 

Marie, P.: “De l’osteoarthropathie hypertrophiante pneumique.” Revue de 
Med., 1890, x, 1. 

Hoffman, V.: “Ein beitrag zur Kenntnis der Osteoartliropathie hyper¬ 
trophiante pneumique (P. Marie).” T>eut. Arch. f. kl. Med., 1919, cxxx, 
201 . 

Frangenheim, P.: “Die Osteoartliropathie hypertrophiante pneumique; 
Neue deut. Chir.,” “ Band x. P. v. Bruns, Ferdinand Enke, Stuttgart, 1919. 


' S." 



e., 


CHAPTER IV 
RICKETS, RHACHITIS 

Rickets is a constitutional disease of infancy and early 
childhood, whose chief anatomical changes appear in the 
bones. Good authority is behind the statement that the 
disease occasionally occurs in foetal life. Certainly its 
manifestations have been observed in very early infancy. 
The so-called “late rickets” of adolescents is probably 
a misnomer. 

^Etiology. —Nothing definite is known as to this. The 
marrow changes point strongly toward chronic infection 
as a cause, and various investigators have claimed to have 
produced the disease experimentally by the use of infec¬ 
tious agents, but their claims have not been substantiated. 
On account ol the similarity of the bone changes in rickets 
and in syphilis, syphilis lias been considered as a cause of 
rickets, but the two diseases are quite distinct. One does 
not cause the other. 

The cause of rickets is closely bound up with the proc¬ 
esses of nutrition. The disease can be produced experi¬ 
mentally in animals, by surrounding them by unnatural 
conditions. The essential element of these unnatural con¬ 
ditions is popularly thought to be an error in diet, an 
absence from the food of some essential element, but 
Leonard Findlay and others stress the importance of con¬ 
finement, and of the lack of fresh air. Perhaps all are 
but contributing causes. 

Rickets is more common in certain races than in others, 
and m ceitain climates than in others. People from 

158 


RICKETS, RHACHITIS 


159 


southern climates, transplanted to northern, are especially 
liable to the disease, possibly because they live more in-doors 
in their new domicile. On the other hand the Esquimaux 
are said to be exempt from the disease. It is much more 
frequent in the city than in the country. It is common in 
England and in Germany, and in our northern cities many 
severe cases are seen among negroes and Italians. 

Pathology. —The bone changes alone interest us here, 
and it is hard to say which is the fundamental change. The 

r~- 



Fig. 52. —Rickets. Low power photomicrograph of the costochondral junction. 

Note the irregularity of outline of the cartilaginous disc on its left border. 

marrow becomes very vascular and undergoes a fibrous 
change. Islands of osteoid tissue appear in it, and the 
Haversian canals widen. In other words the marrow is 
the seat of a chronic inflammation. The most marked 
evidences of the disease are on the outside of the cortex, 
and in the region of the epiphysial disc; in other words, 
in those parts of the bone where growth is most active. 

The changes at the epiphysial line (as at the costo¬ 
chondral junction) are among the most characteristic. 
Masses of marrow tissue push in among the columns of 
cartilage cells in the zone of provisional calcification 
(Nichols). The zone of provisional calcification disap- 



160 INFLAMMATION IN BONES AND JOINTS 

pears, the cartilage cells lose their typical arrangement, 
and the epiphysial disc becomes irregular and decidedly 
broadened. On its diaphyseal side masses of osteoid tissue 
instead oi bone, are laid down, and in this osteoid tissue 
islands of cartilage persist. In other words ossification is 

halted. Neither calcification 
nor ossification takes place. 
Layers of osteoid tissue form 
on the trabeculae of the diapliy- 
sis, but whether or not there is 
ever a reversion of bone tissue 
to osteoid is doubtful. Prob¬ 
ably the process is best inter¬ 
preted as a failure to build up 
bone, rather than an actual 
tearing down of bone already 
built up, aside from the tear¬ 
ing down inseparable from 
the remodelling incidental to 
growth. 

Tlie periosteum is thick¬ 
ened, and layers and arches of 
osteoid tissue instead of true 
bone are formed in it. Rare¬ 
faction of the cortex is pro¬ 
ceeding meanwhile, and the 
Haversian canals are widened and contain vascular mar¬ 
row. The masses of osteoid tissue in the periosteum give 
to the bone a thickened appearance. They are more prom¬ 
inent in certain situations than in others, especially upon 
the parietal eminences of the skull. In other parts of the 
skull absence of bone formation, as well as of osteoid tissue, 
is the prominent feature. This is best seen in the occipital 



Fig. 53.—Skeleton of rickety child • 


RICKETS, RHACHITIS 


161 


bone, the so-called craniotabes. The bone is thin and 
parchment like, easily indented by pressure with the finger. 
This craniotabes is one of the most important diagnostic 
signs of rickets. 

Lack of bone formation in the cranial bones causes a 
persistence of the fontanelles, also an important diag¬ 
nostic sign. 

In gross the bones become soft and bent, and are broad¬ 
ened in the region of their epiphyses. Fractures are said 
to be frequent. Vascular, soft, spongy, grayish-red 
masses of tissue are seen in the medulla and on the cortex. 
The epiphysial line is broadened, and, instead of being 
sharply defined and approximately straight, is irregular. 
Medullary and osteoid tissue extends into it. The central 
medullary canal is widened. 

When the disease has run its course, calcification and 
ossification of the osteoid tissue take place, and the bones 
become denser than normal—sclerosed. The deformities 
may persist or they may disappear. Almost always in 
later life, the enlarged epiphyses and the peculiar shape 
of the head, remain as vestiges of the infantile disease. 

Symptomatology. —The constitutional manifestations 
of rickets are numerous and well known. Among them 
are the nervous symptoms, the convulsions, the laryngismus 
stridulus, the restlessness at night, etc. The patient is 
anaemic and pasty looking, and is afflicted with sweating 
about the head. Usually he is pot-bellied and suffers from 
constqiation. Teething is late and the child does not begin 
to walk at the usual time. 

All these are quite important, but they do not justify 
a diagnosis of rickets. This is only to be made upon the 
bone changes. The two most important of these perhaps 
are the craniotabes and the epiphysial changes, the latter 


n 


162 


INFLAMMATION IN BONES AND JOINTS 


including the changes at the junction of the ribs with 
their cartilage. 

Craniotabes is a very early sign, and by some is consid¬ 
ered as an invariable and pathognomonic sign of rickets, 
provided its presence is carefully sought. It may be more 

or less general in the occipital 
bone, or small areas only may 
be involved. 

The enlarged epiphyses are 
easily detected. The enlarge¬ 
ment of those of the wrist and 
ankle is most evident. The 
enlargement of the costo-chon- 
dral junctions causes a line of 
knobby prominences on the 
chest wall, known as the rhachi- 
tic rosary. 

The new bone on the 
parietal eminences gives rise to 
a peculiar shape of the head— 
a squareness that is quite 
characteristic. The forehead 
is prominent. Some patients 
are dolichocephalic, not square-headed. The occiput is 
usually rather broad and flat. 

Harrison’s groove, the concavity of the lower part of 
the antero-lateral chest wall, is often quite marked in 
rhachitic patients. While not directly caused by the dis¬ 
ease, its formation is evidently facilitated by the softness 
of the ribs. The concavity of the chest is in marked con¬ 
trast to the prominent belly. 

The spine usually has a long rounded convexity. The 





RICKETS, RHACHITIS 


1G3 


deformity may appear more or less fixed, but, if the child 
he laid upon his face, and if his pelvis be lifted from the 
table by raising his heels in the air, pressure with the palm 
of the hand upon the curve will obliterate it. Many of 
the severe cases of rotary lateral curvature are probably 
rhachitic in their origin. The pelvis is often narrowed and 
deformed. The rhachitic pelvis in the female becomes of 
great interest in later life to the obstetrician. 

In the lower extremity the rhachitic deformity takes 
the form of knock knee or how leg. In the former the 
deformity is usually in the femur, in the latter in the tibia. 
Probably the chief cause of these deformities is the inability 
of the bones of the extremity to bear the weight of the 
body without bending, but sometimes they may be quite 
marked in children who have never walked. The popular 
idea that they are caused by too early walking, is of course 
erroneous, for the rickety child usually walks late, and any 
child will always walk as soon as he can. In the active 
stages of the disease, and roughly up to the end of the 
fourth year, these crooked bones have a more or less elastic 
feel when an attempt is made to bend them, but after that 
time they become quite hard and unyielding. As long as 
they are soft there is some hope of correcting the deformity 
with braces, but when they have become eburnated, little 
can be expected from conservative treatment. 

The diagnosis is made on the peculiar bone changes. 
The severe cases rarely give rise to doubt. The milder 
ones are often missed. The disease is very frequent in 
large cities, and, if one is looking for its manifestations, 
one will find them in a very heavy percentage of one’s cases. 

Scurvy has its painful swellings in the neighborhood of 
the joints, its more or less acute onset, and its hemorrhages. 
The rhachitic spine may simulate the tuberculous spine, but 


164 


INFLAMMATION IN BONES AND JOINTS 


it lacks rigidity, muscular spasm and pain. Other signs 
of rickets can be found, and these practically rule out tuber¬ 
culosis, for the association of active rickets and tuberculosis 
is at best very rare. 

In chronic hydrocephalus the shape of the head is globu¬ 
lar rather than square, and the epiphyses are not enlarged. 



Fig. 55.—Rickets. Skiagram of a knee. 

Treatment.— Of the first importance in the active 
stages are a well regulated diet and plenty of fresh air. 
Findlay stresses the importance of exercise, but manifestly 
a child with rhachitic deformities in its lower extremities, 
should be kept off his feet as much as possible. Otherwise, 
unless he wear braces his deformities will increase. Most 
authorities, in addition to a proper diet, recommend the 
administration of cod liver oil. Some of them believe also 
in the efficacy of phosphorus. 




RICKETS, RHACHITIS 


165 


It is seen that the treatment of rickets as a disease, is 
along medical lines. The deformities which follow the 
disease present a different problem. If they are attacked 
early, before the bones become sclerosed, their treatment 
usually is not very difficult. The round back, or the scoli¬ 
otic spine, demands recumbency, preferably on some such 
apparatus as the Whitman-Bradford frame. 

Mild degrees of bow-leg or knock-knee may he treated 
by frequent manipulation. The mother is shown how to 
bend the limb as if it were a crooked stick which she were 
trying to straighten. She should manipulate it fifty or 
a hundred times a day. In addition the sole of the shoe is 
raised about a quarter of an inch, on the inner side for 
knock-knee, on the outer for bow-leg- 

More marked cases demand brace treatment. Stand¬ 
ard forms of braces are in use, but it is not difficult for 
anyone with a little mechanical ability to devise one that 
will answer the purpose perfectly. 

Severe cases of bow-leg and knock-knee demand opera¬ 
tive treatment, as do moderate cases after the bones have 
become hardened, that is, after the end of about the fourth 
year. Osteotomy is not a difficult operation, and if done 
with ordinary care is comparatively free from risk. A sharp 
osteotome incises the tissues longitudinally down to, and 
through, the periosteum, at the seat of the greatest deform¬ 
ity. In bow-legs this is usually at the junction of the mid¬ 
dle and proximal thirds of the tibia, in knock-knee just 
proximal to the condyles of the femur. After the peri¬ 
osteum has been incised longitudinally, the blade of the 
osteotome is turned transversely and with blows of a mallet 
divides partially the bone. The fracture is completed by 
manual force. After every few strokes of the mallet the 
operator moves the osteotome back and forward to keep it 
from wedging fast. 


166 INFLAMMATION IN BONES AND JOINTS 

One or two sutures are inserted in the skin, a sterile 
dressing is applied, and the limb is put up in plaster of 
Paris in a slightly overcorrected attitude. The plaster 
of course extends well above and below the seat of the 
fracture, and remains on for about two months. If the 
bones are still soft, braces should be applied when the 
plaster is removed. 


BONE SYPHILIS 

Badix, Paul-Vital: “Syphilis osseuse hereditaire tardive.” Presse MZd., 1914, 
xxii, 240. 

Baginsky, Adolph: “ Bone lesions of hereditary syphilis in children.” Internat. 
Clin., 1899,. 9 ser., iii, 224. 

Ely, Leonard W.: “A case of bone syphilis masquerading as tuberculosis.” 
Med. Rec., 1912, lxxxi, 1179. 

Fisher, Arthur L., Sypliilitic bone and joint lesions simulating tuberculosis.” 
J. A. M. A., 1917, Ixviii, 366. 

Fitzwilliams, D. C. L.: “Syphilitic affections of bones met with in childhood.” 
Brit. Jour. Child, Dis., 1912, ix, 97. 

Guszmax, Josef: “Polyarthritis syphilitica acuta.” Wien. med. Wchnsclir., 
1915, lxv, 186. 

Hazen, Henry H.: “Syphilis.” St. Louis, C. V. Mosby Co., 1919. 
Hochsinger, Carl: “Syphilis.” Pfaundler und Schlossmann Handbuch der 
Kinderheilkunde, 1910, ii, 437. 

Lohe, H.: Rlinische und pathologisch-anatomische Untersuchungen fiber 
Skelettveranderungen bei kongenitaler Syphilis und ihre Heilungsvor- 
gange.” Virchows Archiv., 1915, ccxx, 95. 

Milian: “Syphilis des os et des articulations.” Nouveau traits de Medicine, 
1912, xxxix, 95. 

O’Reilly Archer: “Joint syphilis.” Am. Jour. Orth. Surg., 1913-14, xi, 431. 
Orth, Johannes: “ Ein Beitrag zur Kenntnis der congenitalen Syphilis.” 

Dermat. Studien Von Unna., 1910, xx, 1. 

Owen, Sydney A.: “Syphilitic diseases of joints and bones in childhood” 
Med, Press and Circ., 1913. cxlvii, 318 

Parrot, M. Jules: “ Les lesions osseuses de la syphilis hereditaire.” Path. 
Soc. Trans., 1878-79, xxx, 339. 

Parrot: “Deux cas de syphilis hereditaire avec lesions osseuses.” Soc. de. 
Biol. Mem., 872, iv, 119. 

Payr, E.: “Syphilis der Gelenke.” Lehrbuch der Chirurgie, Wullstein u. 
Wilms, 912, iii, 521. 

Peritz, Georg: “ Ueber die Syphilis der Wirbelsaule.” Charite Ann., 1913, 
xxxvii, 65. 


RICKETS, RHACHITIS 


167 


Pick, Ludwig: “ Zur Rontgendiagnose der angehorenen Knochensyphilis.” 

Deutsche med. Wchnschr., 1919, xlv, 989. 

Pick, Ludwig: “Zur Rontgendiagnose der angeborenen Knochensyphilis.” 

Deutsche med. Wchnschr., 1919, xxxv, 953. 

Stolper, P.: “ Ueber die Beziehungen zwischen Syphilis und Trauma.” 

Deutsche Ztschr f. Chir. 1902, lxv, 117. 

Taylor, R. W.: “Clinical observations on the syphilitic lesions of the bones 
of the hands in young children.” Arch. Sclent, and Pract. Med., 1873, 
i, 354 

Wallace, James O.: “Diagnosis of syphilis of bones and joints.” Jour. 
Orth. Surg., 1919, i, 258. 

PAGET'S DEFORMING OSTEOMYELITIS 

Connolly, Harry W.: “A case of Paget’s disease.” Med. Jour, of Australia, 
1916, i, 283. 

Czerny, Y.: “ Eine lokale Malacie des Unterschenkels.” Weiner med. 

Wchnschr., 1873, xxiii., 894 

DaCosta, J. Chalmers, Funk, Elmer H., Bergeim, Olaf and Hawk, 
Philip B.: “Osteitis deformans.” Publications from the Jefferson Medical 
College and Hospital, 1915, vi, 1. 

Daser. Paul: “ L T eber einen Fall von Osteitis deformans (Paget’s).” Munch, 
med. Wchnschr., 1905, lii, 1634 

Elsner, Henry L.: “Osteitis deformans (Paget’s disease) including a report 
of two cases.” New York State Jour. Med., 1910, x, 287. 

Ferris, Albert Warren: “A case of osteitis deformans.” Med. Rec., 1919. 
xcv, 852. 

French, Herbert: “A case of osteitis deformans with pronounced affection 
of forearm.” Brit. Jour. Surg., 1919-20, vii, 425. 

Graffner: “ Ein Fall von Ostitis deformans (Paget).” Berliner klin. 
Wochenschrift, 1913, i, 1369. 

Haun, Reginald G.: “A case of osteitis deformans terminating with cerebral 
symptoms.” Brit. Med. Jour., 1910, i, 135. 

Hartmann, Kari: “Zur kenntnis der Ostitis fibrosa (deformans).” Beit, 
zur. klin. Cliir., 1911, lxxiii, 627. 

Heazlit Ledra: “Sarcoma complicating Paget’s disease of bone. Report of 
case.” New York State Jour. Med., 1917, xvi, 331. 

Higbee, William S., and Ellis, Aller G.: “A case of osteitis deformans.” 
Jour. Med. Res., 1911, xxiv, 43. 

Kilner. Walter J.: “Two cases of osteitis deformans in one family.” Lancet 
1904, i, 221 

Kutscha, Ernst von: “ Beitrag zur Kenntniss der Ostitis deformans (Paget’s).” 

Arch. f. klin. Chir., 1909, Ixxxix, 758. 

Lancereaux, E.: “Traite d’anatomie Pathologique.” 1889, 173. 

Lancereaux, E.: “Traite de l’herpetisme.” 1883, 147. 


168 INFLAMMATION IN BONES AND JOINTS 

Locke, Edwin A.: “Osteitis deformans with sarcoma of the humerus.” Med. 
Clin. N. A., 1917-18, i, 947. 

Mackey, Charles: “A case of osteitis deformans with Huntington’s chorea.” 
Lancet, 1906, ii, 787. 

Marie, Pierre et Leri, Andres: “ Le crane dans la maladie osseuse de Paget.” 

Soc. Med. des Hopitaux, 1919, xxxv, 901. 

De Massary et Lechelles: “Maladie osseuse de Paget localisee a un seul os 
long.” 1920, xxxvi, 134. 

Matsuoka, M.: “ Beitrag zur Lehre von der Pagetschen Knochenkrankheit. (Os¬ 
teomalacia chronica deformanshypertrophica nach Recklinghausen).” 
Deutsch. Zeitschrift f. Chir., 1909, cii, 515. 

Packard, Frederick A., Steele, J. D., and Kirkbride, T. S.: “ Osteitis defor¬ 
mans.” Am. Jour. Med. Sci., 1901, cxxii, 552. 

Paget, James: “Additional cases of osteitis deformans.” Med. Chir. Trans . 
1882, lxv., 225. 

Paget, James: “On a form of chronic inflammation of bones.” Med. Chir. 
Trans., 1877, lx, 37. 

Paine, F.: “Case of osteitis deformans.” Royal Jour. Med., 1913, vi, 72. 
Parry, T. Wilson: “A case of osteitis deformans.” Brit. Med. Jour.. 1912, 
i, 879. 

Perkins, C. Winfield: “A Rontgenographic study of osteitis deformans 
—Paget's disease.” American Jour. Rontgenology, 1919, vi, 151. 

Pernet, George: “ Morphoeo-sclerodermia of the shins associated with osteitis 
deformans.” Brit. Jour. Dermatology, 1917, xxix, 110. 

Rathbun, Nathaniel P.: “Report of a case of osteitis deformans.” Am. 
Jour. Surg., 1911, xxv, 66. 

Stahl, B. Franklin: “Osteitis deformans, Paget’s disease, with reports of 
two cases and an autopsy in one.” Am. Jour. Med. Sci., 1912, cxxxxiii, 525. 
Stivelman, B. and Ray, E. L.: “Paget’s disease of the bones.” New York 
Med. Jour., 1918, cviii, 678. 

Thompson, W. Gilman: “Osteitis deformans (Paget’s disease).”3/^?. Rec., 
lxxxiii, 832. 

Vogel, Karl M.: “A case of Paget’s disease. Med. Rec., 1911, lxxx, 214. 
Wallace, Guy: “A case of osteitis deformans.” Bellevue and Allied Hospitals. 
Med. and Surg., Rep., 1911-12, v, 7. 

Watson, William T.: “A case of osteitis deformans.” Johns Hopkins Hospital 
Bulletin, 1898, ix, 133. 

Wilks: “Case of osteoporosis.” Path. Soc. London Trans., 1868-69, xx, 273. 

OSTEOMYELITIS FIBROSA 

Bloodgood, J oseph C.: “ Benign bone cysts, ostitis fibrosa, giant-cell sarcoma 
and bone aneurism of the long pipe bones.” An. Surg., 1910, lii, 145. 
Bockeniieiner, Ph.: “ Ueber die diffusen Hyperostosen der Schadel und 
Gesichtsknochen s. Ostitis deformans fibrosa.” Arch. f. klin. Chir., 1908, 
lxxxv, 511. 


RICKETS, RHACHITIS 169 

Boit: “ Ueber Leontiasis ossea und Ostitis fibrosa.” Arch. f. Min. Chir., 1912, 
xcvii, 515. 

Bullowa, Jesse G. M.: “Osteitis fibrosa.” Med. Rec., 1915, Ixxxvii, 539. 

B orchard. A.: Zur Diagnose der chondromatosen fibrosen und cystiscben 
Degeneration der Knochen.” Fortschr. a. d. Geb. d. Rontgenstrahlen, 1912-13, 
xix, 113. 

Curschmann, H.: “Ueber osteomalacia senilis und tarda.” Med. Klinik, 
1911, vii, 1565. 

Czerny, V.: “ Eine locale osteomalacie des Unterscbenkels.” Wiener Med. 
Wochsch., 1873, xxiii, 893. 

Fujii: “Ein Beitrag zur Kenntnis der Ostitis fibrosa mit ausgedehnter 
Cystenbildung.” Deutsche, f. Chir., 1912, cxiv, 25. 

Gaugele, K.: “Zur Frage der Knochencysten und der Ostitis fibrosa von 
Recklinghausen's.” Arch. f. klin. Chir., 1907, lxxxiii, 953. 

Greig, David M.: “Osteitis fibrosa.” Edinburgh Med. Jour., 1920, xxiv, 324. 
Hartmann, Karl: “Zur Kenntnis der Ostitis fibrosa (deformans).” Beit. z. 
klin, Chir., 1911, Ixxiii, 627. 

Heineke, H.: “Ein Fall von multiplen Knochencysten.” Beit. z. klin. Chir., 
1903, xl, 481. 

Jacoby, Martin, and Sciiroth: “Ueber die Einwirkung von Calcium lacticum 
auf einen Fall von Ostitis fibrosa. . .” Mitteil. a. d. Grenzgel. d, Med. 
u. Chir., 1913, xxv, 383. 

Katholicky: “Ostitis deformans.” Wien. klin. Wochsch., 1906, xix, 1428. 
Koch, Max: “Demonstration eines Schadels mit Osteitis deformans Paget.” 

Deutsche path. Gesell. Verhand., 1909, xiii, 107. 

Kolisko: “Ostitis deformans.” Wiener klin. Wchnschr., 1906, xix, 1429. 

Lake, Norman C., and Schuster, Norah H.: “A case of osteitis fibrosa.” 
Lancet, 1920, i, 546. 

Lotsch, Fritz: “Ueber generalisierte Ostitis fibrosa mit Tumoren und 
Cysten. . .” Arch. f. klin. Chir., 1915-16, cvii, 1. 

Monckeberg: “Ueber Cystenbildung bei Ostitis fibrosa. Verb. der. dent. 
Path. Gesell,, 1904, vii, 232. 

Moizard, and Bourges: “ Un cas d’osteite deformante.” Arch, de Med, Exper., 
1892, iv, 479. 

Oestreich, R.: u. Slawyk, “ Riesenwuchs und Zirbeldriisen-Geschwulst.” 
Virchow’s Arcliiv. 1898, clvii, 475. 

Pfeiffer, C.: “ Ueber die Ostitis fibrosa und die Genese und Therapie der 
Knochencysten.” Beit. z. klin. Chir., 1907, liii, 473. 

Prince, Morton: “Osteitis deformans and hyperostosis cranii. . .” Am. Jour. 
Med. Sci., 1902, xxiv, 796, 

Roth, Max, and Volkmann Joh.: “Zur Kenntnis generalisierten Ostitis 
fibrosa.” Mitteil. a. d. Gremzgeb. d. Med. u. Chir., 1920, xxxii, 427. 
Sutton, Bland: “Leontiasis ossea.” Illus. Med. News , 1889, ii, 217. 


170 


INFLAMMATION IN BONES AND JOINTS 

RICKETS 

Cohn, M.: “ Zur Pathologie der Rachitis.” Jnhrb. f. Kinderheilk., 1893-1894, 
xxxvii, 189. 

Comby, J.: “La radiographie dans le rachitisme.” Arch. de. Med. de enf., 
1918, xxi. 549. 

Findlay, L.: “The etiology of rickets.” British Med. Jour., 1908, ii, 13. 

Findlay, L.: “Rickets: a historical note.” Glasgow Med. Jour., 1919, xci, 14T. 

Findlay, L.: “Rickets in Its relationship to housing.” Glasgow Med. Jour., 
1918, Ixxxix. 268. 

Huldsciiinsky, K.: “Die Ultraviolettherapie der Rachitis.” Strahlentherapie, 
1920, xi, 435. 

Jackson, L.: “Demonstration of micrococci in the bones in rickets and 
scurvy.” Jour. Infect. Dis., 1918, xxii, 457. 

Kassowitz, M.: “Zur Theorie der Rachitis.” Wien. Med. Wchschr., 1901, li, 
1753, 1807, 1857. 

Leri, A. and Beck, T.: “ Le ‘Petit rachitisme’.” Ann. de Med., 1919, vi, 449. 

Looser, E.: “ Ueber Spaetrachitis und Osteomalacie.” Deutsche Ztschr. f. 
Chir., 1920, clii, 210. 

Mellanby, E.: “ An experimental investigation on rickets.” Lancet. 1919, i, 407. 

Oelime, C.: “Ueber die Beziehungen des Knochenmarkes zum neugebildeten, 
kalklosen Knochengewebe bei Rachitis.” Beitr. z. Pathol. Anai., 1908, 
xliv, 197. 

Paton, D. N., and Watson, A.: “The aetiology of rickets.” Brit. Jour. Exp. 
Path., 1921, ii. 75. 

Paton, D. N., and Findlay, L.: “Observations on the cause of rickets.” Brit. 
Med. Jour., 1918, ii, 625. 

Sciimorl, G.: “Ueber Rachitis tarda.” Deutsche Arch. f. klin. Med., 1905-1906, 
lxxxv, 170. 

Schmorl, G.: “Die pathologische Anatomie der Rachitis.” Dresden. Gesellsch. 
f. Natur. u. Heilk. Jahresbericht., 1906-1907, xc. 95. 

Schmorl, G.: “Ueber die Knorpelverkalkung bei beginnender und bei 
heilender Rachitis.” Deutsche Path. Gesellsch. Verhandl., 1905, ix, 248. 

Schwarz, H.: “ Craniotabes and beading of the ribs as signs of rachitis.” 
Am. Jour. Dis. Child., 1920, xix, 384. 

Shipley, P. G., and Park, E. A.: McCallum, E. V., and Simmonds, N.: 

“ Studies on experimental rickets. No. iii.” Johns Hopkins Hosp. Bull., 
1921, xxxii, 160. 

Virchow, R.: “Das normale Knochenwachsthum und die rachitische Stoerung 
desselben.” Arch. f. path. Anat. und Physiologie., 1853, v, 409. 


SECTION IV. 


CHRONIC ARTHRITIS 











" »i 9 S£ B 9| I ■ |HI ■ ■ 

. 










' 


































CHAPTER I 


THE TWO GREAT TYPES 
JOINT TUBERCULOSIS IN GENERAL 

The custom is almost universal to describe the chronic 
arthritides as separate from inflammations in the shafts. 
This custom has decided merit, for, when the joint is 
involved, the symptoms of the arthritis usually dominate 
the picture, and throw the symptoms referable to the bone 
decidedly in the background. The fact must not be forgot¬ 
ten however that the distinction is largely an artificial one, 
that no sharp dividing line can be drawn between an arthri¬ 
tis and a myelitis, that most arthritides are the result of a 
previously existing myelitis, and that a primary arthritis 
may easily spread into the bone and involve the bone 
marrow. 

The whole subject of chronic arthritis is a most confused 
one in all its aspects. Indeed this confusion exists not only 
as to its aetiology and its pathology but also as to its classi¬ 
fication and nomenclature, so that often a student is baffled 
in his efforts to find out an author’s meaning. 

Until comparatively recently practically all these 
arthritides were grouped under the broad general name of 
chronic rheumatism, and were supposed to be due to some 
mysterious dyscrasia or diathesis, and even to this day we 
find some investigators taking refuge in the similar terms 
rheumatoid and metabolic- It is interesting in studying 
chronic arthritis to see how a firm structure of fact slowly 
has been built up by patient investigation. On the other 
hand at all times this structure of fact has been almost 

173 


174 INFLAMMATION IN BONES AND JOINTS 

buried in a flood of supposition and theory. One by one, 
various members of this group of diseases have been identi¬ 
fied and described, until now it may be said that the main 
features of the majority of them are fairly well known, 
and the pathological characteristics of the others. 

Classification.— The prevailing method of classify¬ 
ing the chronic arthritides is partly on an setiological, and 
partly on a pathological and clinical basis. Thus, most 
writers describe tuberculous, gonococcic, syphilitic and 
other forms of arthritis, and then classify the cases of 
unknown aetiology according to some pathological or 
clinical feature which they deem most important. The 
disadvantages of this method are manifest. The ideal 
classification of course is an axiological one, but, as long 
as so much doubt hangs about the cause of several forms 
of chronic arthritis, it is well if possible to classify on a 
clinical or a pathological basis, preferably the latter. As 
has been said, the changes, especially the gross changes 
observed in the tissues of the joint are comparatively few 
in number, and on the basis of these it is possible to divide 
all cases of chronic arthritis into two great divisions or 
types, whose pathological features are sharply differenti¬ 
ated and whose clinical features usually are so well marked 
as to permit a distinction between them. They may be 
differentiated almost invariably, or invariably, with the 
Rontgen ray. The first type is characterized by a pro- 
hfeiative inflammation in the synovial membrane and in 
the bone marrow, with a resulting rarefaction or death 
of the bone, and a perforation or death of the articular 
cartilage. This type probably includes all the bacterial 
arthritides, £•£/•, tuberculous, syphilitic, pneumococcic, ty¬ 
phoid and coccidioidal arthritis j and the cases of chronic 


JOINT TUBERCULOSIS IN GENERAL 


175 


arthritis supposed to be caused by diplostreptococcic infec¬ 
tion in the tonsil, in the deep urethra, and in other locations. 
The English often call these last cases “rheumatoid” ar¬ 
thritis, Goldthwait calls them “atrophic” and “infectious” 
arthritis, Nichols and Richardson call them “the prolifera¬ 
tive form,” and other writers have given them other names, 
almost without number. 

An arthritis of this type may recover completely, or 
it may result in fibrous or in bony ankylosis. All the 
cases in this type are alike, clinically and radiographically. 
They all belong in the same family, so to speak. While 
the different members of the family can be often diagnosed 
clinically, a positive diagnosis can be made only in 
the laboratory. 

The second great type has been recognized as a clinical 
entity for a number of years, though its cause has never 
been established. Its gross pathological feature is the 
formation of new bone at the joint line, with the production 
of spurs and bony ridges at the lines of insertion of the 
capsule, but the essential original pathological change at 
the bottom of this bone production never has been deter¬ 
mined until recently. This is the senile type of arthritis, 
the “arthritis deformans” of the Germans, the “osteo¬ 
arthritis” of the English, the “hypertrophic arthritis” of 
Goldthwait, the “degenerative form” of Nichols and 
Richardson, and the “metabolic” arthritis of certain other 
writers. The joint becomes distorted and mechanically 
damaged, but union of the bones entering into it, whether 
by fibrous or bony tissue never takes place except in the 
spine. On the other hand the bony changes are permanent, 
and a joint once damaged by this form of arthritis probably 
never returns to a completely normal state. 


176 INFLAMMATION IN BONES AND JOINTS 

Into one of these two great types falls every case of 
chronic arthritis. They can usually be distinguished clini¬ 
cally and always by the X-ray. While every chronically 
inflamed joint belongs quite definitely in one class or the 
other, nevertheless in rare instances a patient may show 
signs of the one great type in certain joints, and of the 
other great type in others, but it is doubtful if the involve¬ 
ment is ever synchronous. 


JOINT TUBERCULOSIS IN GENERAL 177 

THE FIRST GREAT TYPE OF CHRONIC ARTHRITIS 
TUBERCULOUS ARTHRITIS 


^Etiology. —The exciting cause of joint tuberculosis 
is, in every instance, the tubercle bacillus. Authorities dif¬ 
fer as to the relative frequency of the bovine and human 
type of the organism as a causative agent. Except in the 
very rare instances of direct infection from the outside, 
practically unknown, the tubercle bacillus must he brought 
to the joint in the circulation . 1 The consensus of opinion is 
that it comes in the blood, either floating free in the blood 
stream or in the embrace of a leucocyte. Friedrich 2 3 4 5 6 main- 
tains that the infection may he through the lymphatics. 
Though occasionally an infected embolus may he the start¬ 
ing point of the disease, a macroscopic plug of infected tis¬ 
sue as a causative agent is probably a great rarity. Marrow 
tuberculosis may be easily produced in laboratory animals 
hv the injection of a pure culture of tubercle bacilli into the 
nutrient artery , 3,4 as well as by carrying them in on a 
platinum loop through a trephine opening in the cortex . >,<5 

Contributing Causes.— Heredity and environment 

•/ 

may be considered together under this heading, for they 
are not always easy to separate in their influence. There 
is a type of physique considered prone to tuberculous 

1 Kappis: “ Beitrag zur traumatischen Tuberkulose.” Dent. med. Woch., 
1910, xxxvi, 1310. 

2 Friedrich: “ Experimentelle Beitraege. u.s.w.” Dent. Zeit. f. Chir. 1899, 
liii, 512. 

3 Mueller: “Experimentelle Erzeugung typischer Knoclientuberkulose.” 
Cent. f. Chir., 1878-79, xi, 317. 

4 Hueter: “Die experimentelle Erzeugung der Synovitis granulosa, etc.*’ 
Dent. Zeit. f. Chir., 1878-79, xi. 317, 330. 

5 Ely, Leoxard W.: “ Lymphoid marrow and tuberculosis; an experimental 
study.” J. A. M. A., 1915, ixv, 1868. 

6 Oliver, Jean: “Early changes following the injection of tubercle 
bacilli into the metaphysis of the long bones of animals.” Jour. Expr. 
Med.. 1920, xxxii, 153. 


12 





178 


INFLAMMATION IN BONES AND JOINTS 


infection—the so-called tuberculous diathesis—and the 
offspring of tuberculous parents is notoriously vulnerable 
to tuberculosis, but how much of this vulnerability is due 
to constitutional predisposition and how much to the infec¬ 
tion spread by careless tuberculous parents is still a subject 
of debate. 

The same uncertainty exists as to the influence of en¬ 
vironment. The disease is rather frequent in the dense 
population of the larger cities, and its frequency has been 
ascribed to the effect upon the constitution of general 
insanitary conditions, but the element of infection here 
also is probably of much greater importance than is the 
lowered vitality . 7 8 9 

Trauma. —As in most diseases of the bones and joints, 
so in tuberculosis, trauma has been considered an important 
element in the causation. The subject has been attacked 
from the experimental side with contradictory results . 8,9 ’ 10 
Clinicians differ markedly in their estimation of the impor¬ 
tance of injury. Some ascribe to it a very prominent role, 
others disregard it entirely. All authorities agree that a 
severe injury, such as a fracture or a dislocation, is prac¬ 
tically never followed by tuberculosis of the bone or joint. 
The injury is a slighter one, such as a “strain” or a sprain. 
Indeed, as we shall see, some writers have maintained that 
the vulnerability of the joints to injury determines the 
location of tuberculosis in their vicinity. On the other . 

7 In this connection the experience of San Francisco is interesting. A 
marked decrease in the number of cases of joint tuberculosis following the 
great tire of 1906 has been noted. 

8 Krause: “ Tuberkulose der Knochen und Gelenke.” Leipzig; F. C. 
Vogel, 1891. 

9 Friedrich : “ Experimentelle Beitraege zur Kenntniss der chirurgischen 
Tuberkulose.” Deut. Zeit. f. Chir., 1891, liii, No. 16. 

10 Honsele: “ Ueber Trauma und Gelenktuberkulose.” Beit. z. klin. Chir., 
1900, xxviii, 659. 





JOINT TUBERCULOSIS IN GENERAL 


179 


hand, the normal joint is built to withstand the ordinary 
injuries to which it is exposed, and it is hard to believe 
that an injury so slight as to escape the notice of the patient 
or of his parents, could be much of a factor. The tendency 
of the patient to ascribe his disease to an injury, must be 
borne in mind, even to an injury long antecedent. Again 
no trauma other than a fracture can possibly affect the 
bone marrow, where joint tuberculosis in the majority of 
cases begins. Sprengel has called attention to the fact 
that those joints which are most often injured, such as the 
joints of the hand and of the foot, are relatively infre¬ 
quently affected with tuberculosis. 

The most reasonable view yet advanced as to the rela¬ 
tion of trauma to joint tuberculosis, is the following: 
Strictly speaking, trauma plays no role in the causation 
of the disease itself. It simply lights up an already exist¬ 
ing, perhaps quiescent, disease. Examination of speci¬ 
mens of bones in the laboratory indicates that tuberculosis 
can exist, perhaps indefinitely in the bone marrow without 
involving the joint. Again, fairly extensive involvement 
of the synovial membrane may give rise to symptoms so 
insignificant as not to draw the patient’s attention to the 
disease; or a tuberculosis of the synovial membrane, possibly 
diagnosed at the time of its occurrence as “rheumatism,” 
or dismissed without a diagnosis, may become completely 
encapsulated and may be forgotten. In such a case trauma 
tears the fibrous adhesions loose, and sets the infectious 
material free in the joint, and the patient naturally dates 
his disease from the injury. The trauma of operation 
seems especially to light up joint tuberculosis, as when an 
inflamed joint is explored for diagnosis, or when an opera¬ 
tion is undertaken with an erroneous diagnosis. 

The sequence of joint tuberculosis on certain acute 


180 


INFLAMMATION IN BONES AND JOINTS 

infectious diseases has often been noted, and these diseases, 
somewhat in the order of their importance, are, in the child, 
measles, whooping cough and scarlet fever, and in the adult, 
pneumonia and typhoid. The consensus of opinion is that 
they lower the patient’s vitality and so predispose to the 
invasion of tuberculosis, but it is far more likely that they 
cause an actual morphological change in the bone marrow, 
which renders it a more suitable pabulum for the tubercle 
bacillus. We know that infections cause profound changes 
in the bone marrow, easily recognized by the naked eye 
or under the microscope, changes which are much more 
easily appreciated than are the somewhat vague terms 
“lowered vitality” and “decreased resistance.” Again, the 
diseases which most depress the vitality are not those most 
often followed by joint tuberculosis. 

Occurrence. —Joint tuberculosis occurs at all ages. 
It is frequent in childhood, but very rare in the first year 
of life, perhaps because the portion of the bone most liable 
to invasion is then largely composed of cartilage, whose 
resistance to tuberculosis is well known. Roevsing 11 main¬ 
tains that synovial tuberculosis is fairly frequent in the 
first year of life. 

The male sex furnishes a small majority of the cases 
of joint tuberculosis, not because it is more liable to trauma, 
but because it is more active. What effect function has 
we shall see later. 

The liability of the various joints to invasion is roughly 
proportional to their size. The sacro-iliac joint, with its 
infrequent involvement, forms an exception to this rule. 
Observers differ somewhat in their statistics, but agree 

11 Roevsing, Th.: “ Ueber tuberculoese Arthritis im fruehesten Kincle- 
salter.” Arch. f. klin. Chir., 1896, liii, 620. 




JOINT TUBERCULOSIS IN GENERAL 


181 


fairly well in the main. According to Whitman 12 the spine 
is most frequently affected, then the hip, then the knee, 
ankle and tarsus, elbow, wrist, and the shoulder. Tuber¬ 
culosis of the clavicular joints is rare, and of the joints of 
the fingers and toes very uncommon, though tuberculosis 
of the shafts of the metacarpals and phalanges is fairly 
frequent in childhood. 

Pathology. —The essentials of the disease are the same 
as are those of tuberculosis anywhere in the body, but its 
course is modified by the presence of the joint cavity and 
of the rigid bony shell. Only two tissues in and about the 
joints are vulnerable to the tubercle bacillus unassociated 
with any other organism, except of course in the case of a 
general miliary tuberculosis, and these two tissues are the 
bone marrow and the synovial membrane . 13 Most authori¬ 
ties agree that the disease may start in either of these 
tissues, but Nichols 14 maintains that the origin is always 
in the bone marrow. Basing my opinion upon analogy, 
upon clinical experience, and upon the examination of 
material in the laboratory, I hold the former view, although 
it must be said that Nichols has made out a strong case. 

Tuberculosis of the shafts of the long bones, except of 
the phalanges and the metacarpals is rare in this country, 
though it is said to be more frequent abroad . 15,16 The 
disease attacks the short and the flat bones, and especially 

13 Whitman, Royal: “Orthopaedic Surgery.” Philadelphia and New York, 
Lea and Febiger, 1919, 6th ed. 

13 Ely, Leonard W. : “Joint Tuberculosis.” New York, Wm. Wood & 
Co., 1911. 

“Nichols, E. H.: “Tuberculosis of the bones and joints.” Tr. Am. Orihop. 
Ass., Philia. 1898, xi, 353. 

38 Frazer, John: “Tuberculosis of the bones and joints in children.” 
London, A. & C. Black 1914. 

36 Friedlander: “Die tuberkulose Osteomyelitis der Diaphysen langer 
Rohrenknochen.” Deut. Zeit. f. Chir., 1904, lxxiii, 249. 



182 


INFLAMMATION IN BONES AND JOINTS 


and with greatest frequency, the ends of the long bones. 
This marked predilection of tuberculosis for the bone in the 
region of the joint has been the subject of much discussion, 
and has been explained on various hypotheses, such as the 
abundant blood supply in the marrow in the vicinity, the 
slowness of the blood stream in the spongy bone, and the 
liability of the bone here to injury. Lexer has advanced 
the ingenious theory that the arrangement of the blood 
vessels in the vicinity of the joint is the cause of the deposi¬ 
tion of the tubercle bacilli. In the young, the arteries 
about the epiphysial disc are largely end arteries, and this 
fact favors the lodgment of the supposititious tuberculous 
embolus. Without entering here into all the details of the 
argument, it is sufficient to say that none of these theories 
furnishes a satisfactory explanation . 17 The enquiry is not 
an idle one. Its correct answer not only is important for 
an understanding of the pathology and of the setiology, 
but also has a bearing on all our ideas on the treatment. 

Tuberculosis flourishes in the region of the joints be¬ 
cause the tubercle bacillus finds there its appropriate food 
supply. While the structure of the marrow is most 
diverse, and while its constituents vary greatly, not only in 
different individuals but also in the same individual at dif¬ 
ferent times; nevertheless the bone marrow is generally 
divided into three main classes, namely lymphoid, fatty, 
and ‘'myxomatous” or fibrous. The resistance of fatty 
and fibrous tissues to an unmixed tuberculous infection is 
well known. These tissues make up the bulk of the two 
kinds of marrow that bear their names, and they are prac¬ 
tically immune to a pure tuberculous invasion. Lymphoid 
marrow, on the other hand, like lymphoid tissue anywhere 
in the body, is vulnerable to the tubercle bacillus. 


37 Vide previous writings of the author on this subject. 




JOINT TUBERCULOSIS IN GENERAL 


183 


In the young practically all marrow is lymphoid. As 
age advances the lymphoid marrow gives place to fatty 
marrow, and this in turn generally to fibrous marrow. 
The change begins in the shaft of the long bones, and the 
lymphoid marrow persists longer in their extremities, 
finally disappearing there as well. This is in the human 
being, of course, and is not true of all other animals. In 
adult rabbits the marrow of the shafts, as well as that of 
the extremities of the long bones, is of the lymphoid variety. 
In the human animal, lymphoid marrow is found in the 
bodies of the vertebrae after it has disappeared from the 
extremities of the long bones. Whether it persists there 
into old age I cannot say of my own knowledge. 

When we study the incidence of bone or rather marrow 
tuberculosis we find that it follows closely the distribution 
of the lymphoid marrow, that is, as long as it is not compli¬ 
cated by a secondary infection, and that where no red or 
lymphoid marrow is, there the bone is immune, or practi¬ 
cally immune, to invasion by the tubercle bacillus. This 
rule applies only to the disease as it occurs naturally, for 
it has been my experience that if a pure culture of tubercle 
bacilli be inserted into the tissues of laboratory animals it 
will grow, no matter how resistant the animal may be, or 
how unfavorable a medium the tissue . 1810,20 

Lymphoid marrow in the adult generally is found in 
the spongy bone, and its presence in the extremities of 
the long bones is dependent upon function in the joint. 
When function is abolished in the joint, the lymphoid mar- 

18 Ely, Leonard W. : “ Lymphoid marrow and tuberculosis,” Jour. Am. 
Med. Ass., 1915, lxv, 1868. 

19 Ely, Leonard W.: “Experimental tuberculosis of muscle. Bone and 
joint studies 1.” Stanford University, Cal., 1916. Published by the University. 

20 Oliver, <Tean: “ Early changes following the injection of the tubercle 
bacillus into the metaphysis of long bones.” Journ. Exper. Med., 1920, xxxii, 
153. 




184 


INFLAMMATION IN BONES AND JOINTS 


row tends to disappear. According to Ollier , 21 Mau- 
claire , 22 and Lagrange 23 after bony union has taken place, 
following a resection, the spongy bone in the neighborhood 
slowly disappears and the cortex thickens. The central 
marrow canals of the adjoining bones slowly lengthen and 
approach each other. Eventually they may j oin, and the 
canalization of the former site of the joint may become 
complete, but this is probably the exception. In some of 
my cases of resected knees I have had the chance to watch 
with the aid of the X-rays the rearrangement of the bone, 
and I have noted this tendency to canalization, but I have 
never seen the canalization complete. 

Another important change which follows a bony anky¬ 
losis, is the complete disappearance of the synovial mem¬ 
brane, as has been mentioned in the general section. 

The reason for the usual site of tuberculosis in the 
ends of the long bones, therefore, is the presence there of 
lymphoid marrow. 

Not only is the relation of lymphoid marrow to tuber¬ 
culosis important for a comprehension of the pathology of 
the disease as it exists in bone, but also its recognition 
furnishes us with a definite principle of treatment, and 
enables us to understand many of the aspects of bone and 
joint tuberculosis hitherto obscure, such as the frequency 
of the disease in children, its recovery after resection, its 
improvement under rest, etc. 

The original tubercle is formed in the marrow in the 
vicinity of the joint. In the short and in the flat bones, 
it may be formed anywhere of course, though even in these 
bones the disease chooses certain favorite sites. In the 
long bones the favorite starting place in children is in the 

21 Ollier : “Diet, encycl. des Sciences MSdicales.” Paris, 1870, page 191. 

22 Mattclaire, P.: “Nouveau traite de Chirurgie.” Paris, 1909, page 235. 

23 Lagrange: Trait6 de Chirurgie/’ Paris, 1901. 




JOINT TUBERCULOSIS IN GENERAL 185 

neighborhood of the epiphysial cartilage, probably on its 
shaft side. In the adult it probably starts nearer to the 
joint line itself, that is, nearer to the actual end of the bone. 

The custom in the past has been rather widespread, to 
regard as the typical original lesion a tuberculous infarct, 



Fig. 56.—Discrete tuberculosis in the bone marrow. Low power photomicrograph. 


which was supposed to give a pyramidal shape to the tuber¬ 
culous process in the bone end, with its base abutting on 
the joint. Possibly the disease occasionally may begin in 
this manner, but here, as elsewhere in the body, it probably 
starts as a solitary tubercle caused by the deposition in 
the lymphoid marrow, of tubercle bacilli, which have been 


186 INFLAMMATION IN BONES AND JOINTS 

brought there either in the embrace of a leucocyte, or else 
floating free in the blood stream. There is nothing differ¬ 
ent in tuberculosis of the marrow and of a lymph node, 
except that the former runs its course enclosed in a rigid 
shell, and usually in the neighborhood of a joint. 

From the time of the formation of the original tubercle, 
the disease tends to spread at the periphery, with the same 
tendency to the formation of fresh tubercles, and to break¬ 
ing down as is observed in other organs. Nature on her 
part tries to wall it in with fibrous tissue and, to a lesser 
extent, with bone, and according as one or the other of 
these processes prevails, the disease tends to spread or to 
recover. It is quite possible that many cases of marrow 
tuberculosis are healed by nature without ever having been 
recognized clinically, as are many cases of pulmonary 
tuberculosis. The symptoms are not marked unless the 
disease is in the neighborhood of a joint. In fact, we know 
well that when bony union follows the resection of a tuber¬ 
culous joint, provided only that a pus infection be not 
added, even large amounts of tuberculous tissue left behind 
at the operation are without significance, and may remain 
locked up in the bone indefinitely, causing no symptoms 
unless they are brought back into activity by operative 
measures. 

Starting in the end of the bone the disease may spread 
in any direction, and generally as far as the lymphoid 
marrow extends, though of course it must be said that 
authorities still differ as to the role of the lymphoid marrow 
in the process. It may extend shaftward, or outward 
toward the periosteum. In the latter case the tuberculous 
granulations may break through the thin cortex and the 
periosteum, and eventually gain the surface without joint 
involvement. This is rare, very rare. Tuberculosis seems 


JOINT TUBERCULOSIS IN GENERAL 


187 


to seek the joint as if with a well-defined purpose, taking 
such a path and affecting the bone and the cartilage in 
such a way, and causing such clinical symptoms that one 



Fig. 57—Tuberculosis in the bone marrow immediately beneath the articular 
cartilage, low power photomicrograph. Note the degeneration of the cartilage 
at its surface, the “fingers” of tuberculous granulations pushing up into it, the 
osteoid tissue beneath this, and the rarefied bone at the bottom. 

can make a fairly reliable diagnosis of the disease by its 
effect upon the bone as revealed by the Rontgen rays. 

The tuberculous granulations may reach the joint by 
breaking through at the margin of the cartilage where it 
joins the ligament; or, spreading along under the cartilage, 
they may destroy its nutrition in spots, kill the cartilage, 
and push up through it in the shape of little fingers or 
columns; or, they may spread under wide areas of it, and, 
killing it in whole or in part, cast it off a loose body in the 


188 


INFLAMMATION IN BONES AND JOINTS 


joint. When the infection has burst into the joint cavity 
the synovial membrane becomes affected, and a tuberculous 
arthritis is added to the tuberculous myelitis. 

The next step is the invasion of the other bone or the 
other bones of the articulation. Normal cartilage, carti- 



Fig. 58.;—Joint tuberculosis, low power photomicrograph. The tuberculous gran¬ 
ulations in the marrow have run along beneath the cartilage and dissected it off. Note 
the almost complete absence of bone immediately beneath the cartilage, and the 
degenerated shaggy appearance of the surface of the cartilage. 

lage whose nutrition has not been disturbed, is an absolute 
bar against the march of tuberculosis. The articular 
cartilage draws its nutrition from the marrow beneath it, 
probably to a small extent from the vessels at its circum¬ 
ference, and perhaps also from the joint fluid. It is there- 





JOINT TUBERCULOSIS IN GENERAL 


189 



Fig 59 —Tuberculosis of the knee-joint in a child, with secondary infection Low power 
photomicrograph of the distal end of the femur. The picture shows the* “^l^disc 

granulations, E, E, in the metaphysis make their way at the marpn of the epiphyseal, disc, 
C, into the epiphysis, B, and run along under the articular cartilage, A, killing it and per 
forating it to gain access to the joint. D, periosteum. 


fore practically immune to invasion from the joint side. 
The disease must make its way into the bone at the circum- 




190 


INFLAMMATION IN BONES AND JOINTS 


ference of the cartilage, where it is joined by the tuber¬ 
culous synovial membrane. A process similar to that in 
the marrow of the other bone is then enacted here. 

At any time in the course of the disease a tuberculous or 
cold abscess may form in the bone or in the joint, rupture 
the capsule, gain the surface and become infected. As we 
have seen, simple uncomplicated tuberculosis is a disease 
of lymphoid marrow and of the synovial membrane, follow¬ 
ing certain paths, and never involving other tissues. With 
a secondary infection the whole typical picture changes, 
and the mixed infection may run riot through all the tissues 
in and about the joint. 

When the disease starts in the synovial membrane it 
may stay indefinitely in this structure, involving the entire 
membrane or only a part of it according to circumstances, 
or at any time it mav invade one or more bones of the articu- 
lation, spreading under the margin of the joint cartilage 
where it fuses with the synovial membrane, to gain access 
to the marrow. From then on the progress of the disease 
is the same as in a case with a so-called bone focus. 

We see then that it is perfectly possible to have a tuber¬ 
culous osteomyelitis without an arthritis or synovitis, and 
probably also a tuberculous synovitis or arthritis without 
an osteomyelitis. 

Marrow Changes. —The favorite starting point of the 
disease in the child probably is not, as is often said, in the 
epiphysis, but just to the shaft side of the epiphysial disc. 
In the adult, the primary focus may be anywhere in the 
end of the bone, but other things being equal, it chooses a 
site where the bone is least dense. We speak very posi¬ 
tively of the site of the original focus, but of course it is 
largely a matter of surmise, based upon the X-ray findings 


JOINT TUBERCULOSIS IN GENERAL 


191 


and upon the examination of the material removed at opera¬ 
tion. Often some part of the bone will show an involve¬ 
ment out of all proportion to that of the rest, and we assume 
this to be the original focus. 

There is nothing characteristic about the shape of the 
tuberculous process. It may be wedge shape, with the 
base toward the joint, but in the vast majority of cases it 
is not. If it has a characteristic in this respect, it is irregu¬ 
larity. The tubercles may be discrete, and scattered 
widely through the marrow, or larger and smaller portions 
of the marrow may be nothing but masses of tuberculous 
granulations. Here, as elsewhere in the body, some cases 
show a marked tendency to rapid spread, with diffuse inva¬ 
sion, and necrosis and breaking down—cheesy degeneration 
—while the slower, more benign cases are characterized by 
fibrous encapsulation and discrete tubercles. Fibrosis of 
the marrow may be regarded as nature’s protective reaction. 
It often reaches a considerable degree. A fatty change is 
especially prominent in the old cases complicated by a 
secondary pus infection—the so-called fatty osteomalacia. 
In old cases calcification of the necrotic material is often a 
prominent feature, and this calcified material is responsible 
for the shadows seen in the X-ray plate—shadows some¬ 
times mistaken for new bone. Xew bone formation is 
never a feature of joint tuberculosis, though occasionally 
about old, healed, or almost healed foci, new bone, never 
enough to show in the X-ray plate, may be seen in the 
laboratory specimen. 

The blood vessels of the marrow often show thickened 
walls. The engorgement, so prominent in acute infections, 
is not seen. More or less peculiar to tuberculosis is the 
hand of osteomyelitis immediately under the joint carti¬ 
lages. The results of this upon the bone and cartilage 









192 INFLAMMATION IN BONES AND JOINTS 

often cause a picture which enables one to diagnose the 
disease fairly accurately with the Rontgen rays. 

Healthy marrow may of course be found in the midst 
of diseased. Hence we are not justified in ruling out 



Fig. 60.—Tuberculosis of the metacarpo-phalangeal joint, with 
secondary infection. Note the absence of the cartilage, the marked 
involvement of the bone marrow at the articular surface, and the 
long streamers in the synovial membrane. 

tuberculosis from an examination of one small piece of bone 
in the laboratory. Often an extended search is necessary. 

Bone Changes. —All changes in the bone are to be 
regarded as passive, the result of changes in the marrow. 
The characteristic change is a rarefaction. The bone 




193 


JOINT TUBERCULOSIS IN GENERAL 

trabecula* become thinner and scantier, and more permeable 
to the X-rays. In the milder cases, especially if they have 
had efficient treatment, this may be the only change 
observed. If the disease be more severe the bone is killed. 
It dies in small pieces—the so-called bone sand—or in large 
pieces—sequestra. A sequestrum consists of dead bone 
and dead marrow, may be of any size or shape, and some¬ 
times is found fairly well encapsulated by the surrounding 
bone. It may remain indefinitely at the site of its forma¬ 
tion, and need not be cast off like the sequestrum of a sup¬ 
purative osteomyelitis, though it is doubtful if blood vessels 
ever can push their way into it, absorb it, and replace it 
with new bone. 

In old cases, especially in those complicated by a pus 
infection, the bone may become so thin and soft that it can 
be cut with a knife. Contrary to what one would expect 
in such circumstances fracture is extremely rare in tuber- 
culous bones, so rare that its presence in a suspected case 
speaks strongly against the diagnosis of tuberculosis. 

A tuberculous focus in the end of a young child’s bone 
sometimes stimulates the growth of bone in the neighboring 
epiphysial disc, but this stimulation is never great, and is 
only temporary. Thereafter growth lags behind, and 
when full stature has been attained, the affected limb is 
almost invariably shorter than its fellow. The resulting 
shortening may be due to one or all of three things, viz., 
to subluxation, especially of the hip or knee, to damage to 
the bone in the epiphysis or to the epiphysial cartilage, and 
to the atrophy of disuse. 

Rarefaction is not confined to the bone in the region of 
the affected joint, but is observed also in all the bones of the 
extremity. This is the atrophy of disuse. In this atrophy 

13 


194 


INFLAMMATION IN BONES AND JOINTS 


all the tissues of the extremity share. The muscular 
shrinking is especially noticeable, and accentuates the 
appearance of the swelling in the joint. 

Under the microscope the bone is seen to be less dense 
than normal, and the trabeculae to be scantier and more 
slender. Typical rarefying ostitis, with its classical so- 
called osteoclasts in Howship’s lacunae, is not as frequent 
as one would expect. Instead the trabeculae are often 
edged by cells with the appearance of osteoblasts. Some¬ 
times these cells are separated from the trabeculae by a 
translucent zone, presumably bone undergoing absorption. 

As a rule in the more benign cases, bone absorption 
exceeds bone necrosis. It prevails especially in the zone 
immediately under the joint cartilage. The bony buttress 
disappears, and the cartilage lies upon an irregular band 
of tuberculous granulation tissue, containing a few small 
remnants of bone trabeculae. 

The J oint Cartilage.— The cartilage is roughened, 
irregular and fibrous. It may be dead in whole or in part. 
It may lie on the bone end, scarcely attached here and 
there or it may be loose in the joint. Parts of it, though 
badly damaged, may still remain, while other parts have 
been replaced by tuberculous granulations springing from 
the marrow beneath. Areas of bare bone are not seen, as 
in the second great type of chronic arthritis. 

These cartilage changes are so constant in tuberculous 
joints that they are regarded as characteristic of the disease, 
but they are shared by all the members of the first great 
type of chronic arthritis, though they are rarely present 
in as pronounced a degree. On the other hand they may 
be absent altogether. Occasionally one opens a tuber¬ 
culous joint at operation, and finds the cartilage smooth, 
glistening, and apparently normal. Sometimes the pres- 


JOINT TUBERCULOSIS IN GENERAL 195 

ence of a focus in the bone will be betrayed by a small 
dimple or irregularity in the overlying cartilage. 

The joint cartilage is lessened in area by the encroach- 


m % 



Fig. 61 . —Photomicrograph, low power, from a case of tuberculous arthritis. 
Cartilage above and to the left, synovial membrane below to the right. Note the 
excellent condition of the cartilage, and the extensive involvement of the synovial 
membrane. Apparently the disease is just beginning to make its way into the 

bone at the circumference of the cartilage. 

ment of the synovial membrane at its periphery. Its sur¬ 
face has a fibrous appearance, especially near its margin, 
and may be vascularized—the so-called tuberculous pan- 






196 INFLAMMATION IN BONES AND JOINTS 

nus. This fibrous condition of the cartilage, this pannus, 
was formerly regarded as the result of the organization of 
layers of fibrin precipitated from the joint fluid, but the 
influence of any fibrin deposited upon the cartilage is prob¬ 
ably negligible. The fibrillation is usually most prom¬ 
inent at and near the surface of the cartilage, and is the 
result of three things, viz., absence of function, disease in 
the subjacent bone marrow, and, at the periphery, sub¬ 
stitution of the cartilage by the synovial membrane. 
Under the microscope the fibrillation often can be plainly 
seen. As a rule, the cartilage is also thinned, and this 

decrease in thickness is evident in the X-ray film as an 

%/ 

approximation of the articulating bones. 

The synovial membrane is often thickened, succulent 
and inflamed. At its surface it undergoes a villous prolif¬ 
eration, and the villi may increase enormously in number 
and size, sometimes branching like moss on a rock. The 
resulting condition is sometimes known as lipoma arbores- 
cens. In old, slow cases the synovial membrane may con- 
sist of little else than fibrous tissue. It is seen, therefore 
that tuberculosis is a typical villous arthritis. 

Histologically the membrane presents the typical 
appearance of tuberculosis, sometimes in the shape of dis¬ 
crete tubercles, sometimes as diffuse tuberculous infiltra¬ 
tion. A fair guess as to the clinical course of the case can 
be made from an examination of the stained slide in the 
laboratory. The slow, more benign cases as a rule show a 
marked tendency to discrete tubercles, with encapsulation 
by fibrous tissue, while the more rapid, severe cases show 
diffuse infiltration, with caseation, and with little effort 
at fibrous encapsulation. It is this difference in nature’s 
reaction that is responsible for the various elaborate classi¬ 
fications of tuberculosis. They are of doubtful value. 


JOINT TUBERCULOSIS IN GENERAL 


197 


The borders of the synovial membrane extend at the 
expense of the articular cartilage especially at the surface, 
and in addition the enormously hypertrophied membrane 
may almost conceal the cartilage, but, contrary to general 
teaching, adhesions between the two are not a prominent 
feature of the disease. On the other hand, when the carti- 



Fig. 62.—Tuberculosis of the head of the radius; photograph of the stained slide, x about 6 
diameters. Note how the tuberculous granulations in the marrow have sprouted through the 
articular cartilage at about its middle, and how the articular cartilage has been destroyed at 

the right. 

lage has been thrown off, dense adhesions may form between 
the synovial membrane and the bone marrow. 

The joint usually contains fluid. In the early stages of 
a marrow focus, before the disease actually has communi¬ 
cated with the joint, aspiration may perhaps reveal the fact 
that the fluid is sterile . 24 This is the so-called sympathetic 
synovitis, and is very rare if it ever occurs. The fluid 
usually contains tubercle bacilli, not in great numbers 
perhaps, and often found with difficulty by immediate 
examination, but capable of producing the characteristic 
lesions, when injected into the abdomen of the guinea-pig. 

24 This statement is made on the authority of others. I am not sure that 
I have ever seen such a case. 










198 INFLAMMATION IN BONES AND JOINTS 

The fluid in a tuberculous joint may be serous, hemor¬ 
rhagic, turbid or flocculent. Sometimes it may resemble 
pus, and it may contain detritus of bone and of cartilage. 
In other words, the joint may constitute a tuberculous or 
cold abscess. When a secondary infection is added, the 
joint is an abscess cavity. In the absence of a pus infec- 



Fig. 63.—Low power photomicrograph of the central gap shown in the preceding figure. 

I he marrow, the bone and the cartilage are dead. 


tion, the fluid may be absorbed by nature, but in the pres¬ 
ence of a secondary infection, this of course is impossible. 

In the slow, dry cases, no fluid can be demonstrated in 
the joint, but the joint cavity is replaced by a dense mass 
of fibi ous adhesions, which bind one bone of the articulation 
to the other, and both to the fibrous capsule. These fibrous 
adhesions, this scar tissue, are the result of the proliferative 
inflammation in the bone marrow and in the synovial mem¬ 
brane, and represent nature’s effort at cure by destroying 





culous and cheesy material, capable of lighting up afresh 
an apparently cured disease if trauma or ill-timed operation 
set them free. Indeed I have seen the removal of cheesy 
material from the soft tissues in the vicinity of a knee which 
I had resected for tuberculosis ten years previously, and 
in which firm bony union, with prompt recovery from the 
disease in the bone had resulted. 

The slow, dry cases with dense fibrous adhesions, some- 


Fig. 64. —Synovial tuberculosis, low power photomicrograph. The slow 
benign form, with discrete tubercles and encapsulation. The general course 
of the disease could be guessed with reasonable accuracy from the appearance 
of the stained slide from which this was taken. 


JOINT TUBERCULOSIS IN GENERAL 199 


the joint, but the effort is rarely successful in the absence 
of a secondary infection. Bony ankylosis seldom, if ever, 
results from a purely tuberculous infection. 

A careful search through the mass of dense fibrous 
tissue will often reveal encapsulated collections of tuber- 





























200 


INFLAMMATION IN BONES AND JOINTS 


times are spoken of as “caries sicca, the cases with profuse 
production ot sott granulations in the synovial membrane, 

A 



cig. 05.— 


term. There is here but d|Cse"|fil\t tio“! wi'th chjesy 


as “joint fungus.” Certain of the latter type of cases, 
especially in the knee and in the elbow, are characterized 


JOINT TUBERCULOSIS IN GENERAL 


201 


by marked swelling. The superficial tendon sheaths are 
said to he involved. The muscles in the limb above and 
below the affected joint atrophy greatly, the skin over the 
joint becomes blanched, and the superficial veins prom¬ 
inent. This is the so-called tumor alhus or white swelling. 

Certain writers distinguish various pathological classes 
into which they divide tuberculosis in bone. There seems 
little more practical or scientific reason for this in disease 
of the hone than in disease of the lung or lymph node. 
Thus, the “infiltrating tuberculous lesion” is probably one 
in which nature’s reaction of encapsulation is feeble, the 
“encysted tuberculous lesion’’ one in which it is strong. 
The whole form that the lesion takes is simply the result 
of the balance between the virulence of the infection and 
nature’s power to resist it. 

Rice Bodies are small, smooth, whitish, glistening, slip¬ 
pery bodies, like rice kernels or melon seeds, found some¬ 
times in the milder forms of synovial tuberculosis of joints 
and of tendon sheaths. They may he few in number or 
many. Occasionally a collection of them is found in a 
capsule, hut usually they are loose in the joint. They 
consist of fibrin and connective tissue, and may be attached 
by a pedicle to the capsule of the joint. 25,26> 27,28,29,50 - 


- 3 Goldmann, E. E., “ Ueber die Bildungsweise der Reiskdrperchen, etc.” 
Beit. z. kiln. Chir., 895-96, xv, 757. 

20 Goldmann, E. E.: “Ueber das reiskoerperchenhaltige Hygrom der 
Sehnenscheiden.” Ziegler's Beitraege, 1890, vii, 299. 

27 Garre, C. : “Die primaere tuberkuloese Sehnenscheidentzuendung.” 
Beit. z. klin. Chir., 1890-91, vii, 293. 

28 Landow, M.: “Ueber die Bedeutung des Faserstoffs und seine Um- 
wandlung beim chronischen, insbesondere tuberkuloesen Hydrops fibrinosus.” 
Archiv. f. k. Chir., 1893-94, xlvii, 376. 

20 Riese, H.: “Die Reiskoerperchen in tuberkuloes erkrankten Synovial- 
saecken.” Deut. Zeit. f. Chir., 1895, xlii, 1. 

30 Koenig, Bedeutung: “Bedeutung des Faserstoffs fuer die pathol-anat. 
und klin. Entwicklung der Sehnenscheidentuberkulose.” Cent. f. Chir., 1886, 
xiii, 425. 



202 


INFLAMMATION IN BONES AND JOINTS 


A tuberculous or cold abscess is a collection of broken 
down, necrotic material to which have been added serum 
and leucocytes. But for the presence of tubercle bacilli it 
is sterile. It may be formed in the bone and break into 
the joint, or it may form in the joint itself. It slowly 



a G >J ". L°w P° w er photomicrograph of an incapsulated old cheesy collection 
dug out from the fibrous adhesions in an ankle joint after a resection of the 
talus. 1 he patient gave a history of treatment for tuberculosis many years 
before, supposed to have been cured by conservative treatment. The clinical 
diagnosis was tuberculosis, the laboratory report read “chronic arthritis, no 
tuberculosis. The finding of the tubercle clinched the diagnosis. 


increases in size, unlike a true abscess causing no constitu¬ 
tional reaction, ruptures the capsule, and makes its way 
into the surrounding tissues. It may then gradually dis¬ 
appear completely, or it may make its way slowly toward 
the surface, its course determined by gravity and by the 
path of least resistance. At any time, but especially as 
it nears the suiface, it may be infected secondarily by 


JOINT TUBERCULOSIS IN GENERAL 


203 


pus producing organisms. It then ceases, of course, to be 
a cold abscess. 

The wall of a cold abscess is composed of the necrotic 
tissues in which it lies. When the abscess is secondarily 
infected it contains tubercles. 

When an uninfected cold abscess ruptures spontane¬ 
ously, or is opened with a knife, it discharges its contents, 
and its soft walls fall together. Almost invariably then, 
after a few days, and even in spite of the greatest care, 
secondary infection takes place, and the whole picture 
changes. To the accompaniment of a severe constitutional 
reaction, high fever, etc., a profuse, foul discharge starts 
up, and the abscess walls become thickened, infiltrated and 
“porky.” The original focus deep in the bone is then in 
direct communication with the surface through a longer 
or shorter sinus, with the secondary infection running 
throughout its entire length. The condition now present is 
that of an infected cavity deep in the bone, whose walls 
cannot close in. Suppuration may go on indefinitely, and 
at the last may cause the death of the patient, with its com¬ 
plications of amyloid degeneration, tuberculosis of the 
viscera, or exhaustion. Meningitis, pulmonary tuber¬ 
culosis, etc., are much more frequent in the presence of 
a secondary infection, than otherwise. 

The role of the ligament and of the periosteum is not 
an important one in joint tuberculosis. Both play a pas¬ 
sive part. The ligament, especially in cases treated with 
traction, may become loose and render the joint rather 
unstable. Again, in cases with much deformity, especially 
in the knee, the ligament may become shortened, and make 
the reduction of the deformity difficult or impossible. 

Symptomatology. —Pain is an early and constant 
symptom of joint tuberculosis, and is usually the cause 


204 


INFLAMMATION IN BONES AND JOINTS 


of the patient’s call for medical help, though occasionally 
cases are seen in an advanced stage, that have been prac¬ 
tically painless. The pain is more severe in children as a 
rule than in adults and with bone disease than with synovial. 
It is wont to be sharp, and sometimes comes on in severe 



Old calcified tubercle in the bone marrow. It is this calcification 
in old cases of marrow tuberculosis that is responsible for the shadows in 
tne x-ray picture sometimes erroneously considered as new bone formation. 

Low power photomicrograph. 

paroxysms. It may be felt at the seat of the disease or it 
may he referred. Generally, use makes it worse, but on 
the other hand there is a certain stiffness and pain, almost 
characteristic of tuberculosis, which is experienced in the 
morning for a while after the patient rises, and then disap¬ 
pears when the joint is used. This phenomenon is peculiar 
to the early stages of the disease. 



JOINT TUBERCULOSIS IN GENERAL 


205 


The pain may be worse at night, coining on when the 
muscular spasm relaxes which has held the joint quiet. 
The patient cries out in his sleep, perhaps awakes, and then 
falls asleep again—the so-called night cries, or night ter¬ 
rors. The pain may intermit or it may he constant. 

Sensitiveness to pressure often can he elicited if the 
joint is near the surface and if the synovial membrane can 
be reached by the finger. An inflamed synovial membrane 
almost always is sensitive to pressure. 

Swelling and change of contour also are early and 
prominent signs if the joint lie near the surface, but if it be 
deeply located, as in the case of the hip or the spine, they 
will be evident only in the later stages, if at all. The 
swelling is caused by the fluid in the joint, by the thickening 
of the capsule, and by the infiltration in the surrounding 
tissues, never by bony thickening. The swelling tends 
to assume the classical fusiform shape in time, and is 
accentuated by the atrophy of the muscles above and below 
the joint. According as the amount of fluid or of granu¬ 
lation tissue predominate, the swelling will be fluctuating 
or boggy. It may be increased by abscess formation. 
Especially in disease of the shoulder joint, less often in 
disease of the knee, swelling may be absent. 

Coincident with the pain, or appearing shortly after 
or before it, the function of the member becomes impaired. 
If the disease be in the lower extremity, the impairment 
will manifest itself by a limp, if in the upper, the arm or 
hand will suffer disability, if in the spine, the patient will 
he awkward, and will have difficulty in moving about, 
turning his head, bending, etc. When the joints of the 
spine or of the lower extremity are affected in very young 
children who have walked for only a short time, the patients 
may stop walking. 



206 


INFLAMMATION IN BONES AND JOINTS 


Limitation of motion is perhaps the earliest and most 
important physical sign. This is of course what one would 
expect. Disturbance of function is perhaps the first sign 
of inflammation in any organ, and motion is the function 
of a joint. The limitation is caused by pain, by muscular 
spasm, and by the mechanical obstruction of the inflamma- 



*ig. 68. Old, well incapsulated tuberculous focus found immediately 
beneath the joint cartilage. At the right is the joint cartilagf Below 
is apparently normal bone marrow, above this, thickened bon?trabecuST 
above this fibrous tissue and at the top the old tuberculous foe Js The 
presence of this focus was indicated by a dimple in an apparently normal 
cartilage on the condyle of the femur from a resected knee. 


tory changes in the joint structures. At first merely a 
restriction at extremes, it later increases, and finally may 
amount to a practically complete ankylosis. When the 
limitation is caused by muscular spasm, it disappears under 
a genei al anaesthetic; when caused by anatomical changes, 

it remains even under complete narcosis unless force be 
used to overcome it. 


JOINT TUBERCULOSIS IN GENERAL 


207 


Muscular spasm is a most significant physical sign. 
It is one of the first to appear, and is almost constant. Its 
disappearance usually means the subsidence of activity of 
the inflammatory process. It represents nature’s effort 
to hold the joint at rest, and is responsible for much of the 
stiffness and pain, and also for much of the impairment 
of function and the deformity. Formerly regarded as a 
pernicious symptom to be actively combated, like the pain 
and the disturbance of function the muscular spasm should 
be viewed rather as the evidence of nature’s attempt at 
cure—as a conservative process. Muscular spasm is more 
pronounced in the bony type of the disease than in 
the synovial. 

Early atrophy of the muscles moving the joint is fairly 
characteristic of joint tuberculosis, but not of the pure 
synovial disease. It is doubtless partly an atrophy of dis¬ 
use, but this hypothesis does not explain the excessive 
muscular atrophy in tuberculosis as compared with other 
forms of arthritis. In the late stages of the disease the 
atrophy of an entire extremity may attain great propor¬ 
tions, especially when the case is treated by methods which 
abolish function in the affected extremity, but on the other 
hand, in hip disease treated by the method of weight bearing 
and the short spica, one sometimes sees an actual increase 
in the calf on the affected side—probably on account of the 
vicarious work it is called on to do. 

Deformity may be said to be the sum of the muscular 
spasm, the swelling, the change of contour, the atrophy, 
and the bone destruction. In the early stages it may be 
slight, and only to be distinguished by careful inspection 
and by measurement. Each joint has peculiarities in the 
matter of deformity, but the general attitude of a tuber¬ 
culous joint is semi-flexion. As time goes on the deformity 



208 INFLAMMATION IN BONES AND JOINTS 

increases, and the flexion becomes more extreme, until at 
length subluxation results. Nature seems to be endeavor¬ 
ing to dislocate the joint, but in point of fact, she seldom, 
if ever, succeeeds. At first the deformity can be easily 
corrected, especially with the aid of an anaesthetic, but later 



Fig. 69. —Higher power photomicrograph of a portion of the wall of the old tuberculous 
focus shown in the preceding illustration. This shows nature’s method of walling in the 
disease. At the right is normal bone and marrow. Next to this come thickened bone trabec¬ 
ulae and then dense fibrous tissue. 

the ligaments become accommodatively shortened, and the 
muscles also in their contracted attitude, and a firm con¬ 
tracture ensues, which can only be corrected with the aid 
of the knife, or by prolonged stretching. 

A tuberculous or cold abscess may be regarded as a 
complication, or as a physical sign of the disease. Present 





Fig. 70.—Low power photomicrograph of a portion of a collection of rice bodies 
found incapsulated in the synovial membrane from a resected knee. The 

capsule shows above. 

surrounding structures. Without any effect upon the 
constitution, and, when uninfected, by itself not influencing 
the course of the disease in the slightest, yet its presence 
bespeaks a severe form of the disease, or a feeble resistance 
of the patient, carries a threat of secondary infection, and 
immediately puts the outcome in doubt. 

A cold abscess in a superficial joint like the knee or 


JOINT TUBERCULOSIS IN GENERAL 209 


in a large proportion of cases, it is essentially a phenomenon 
of the late stage, and yet it may be the first thing in rare 
instances to draw the patient’s attention to his malady, 
and to point the medical man to the diagnosis. It is pain¬ 
less and causes symptoms only by pressure upon the 


14 




£10 INFLAMMATION IN BONES AND JOINTS 

the ankle is not difficult to recognize, but one that has 
broken its way through the anterior common ligament of 
the thoracic or lumbar spine, and has made its way along 
the fascial planes into the thigh, may occasion a wrong 
diagnosis unless one is on one’s guard. It appears as an 



Fig. 71.—Photomicrograph of one of the rice bodies shown in the preceding 

figure, rather high power. 

elastic, fluctuating, painless swelling, at first deeply situ¬ 
ated, later gradually approaching the surface, and is diag¬ 
nosed by establishing the presence of a tuberculous focus 
in the spine and then by aspiration. A cold abscess from 
broken-down retroperitoneal glands is diagnosed by ex¬ 
cluding spinal disease, and then by aspiration. 

A cold abscess which has ruptured spontaneously, or 




JOINT TUBERCULOSIS IN GENERAL 


211 


has been opened with the knife, and left open, almost invari¬ 
ably becomes infected by pus germs, and takes a very long 
time to heal. Sometimes it runs for years. It communi¬ 
cates with the surface by sinuses whose mouths present a 
pale, puffy, unhealthy appearance, and which have a ten¬ 
dency to burrow in every direction. 

Tuberculosis of a joint, uncomplicated, does not affect 
the general health. Often the patient has the typical 
appearance that makes one suspect tuberculosis, but per¬ 
haps just as often he appears perfectly strong and vigorous, 
especially if he be an adult. Patients with simple joint 
tuberculosis in favorable surroundings are often plump and 
well throughout the whole course of the disease. Fever 
is not a symptom of the disease. Its presence means the 
advent of a secondary infection, or of some complication 
such as meningitis or pulmonary tuberculosis. 

Diagnosis. —A good working diagnosis can be made 
with a reasonable degree of certainty on carefully weighed 
clinical evidence, but one must never forget that certainty 
is not to be secured without the demonstration of the tuber¬ 
cle bacillus. Chronic inflammation of a single joint, slowly 
growing worse, without evidence of venereal infection or 
fracture is probably tuberculous, especially in a child. 

Rontgen rays show an irregular rarefaction of the 
bones in the vicinity of the j oint, with thinning of the carti¬ 
lage, and sometimes irregularity of the joint surface. In 
a young child the process starts usually on the shaft side of 
the epiphysial cartilage. In addition a carefully taken 
plate may show thickening of the capsule. 

The ordinary tuberculin tests are not of great value, 
but a positive focal reaction with old tuberculin is more 
reliable. The patient is put to bed, and his temperature 
is taken every two hours for twenty-four hours. An intra- 


INFLAMMATION IN BONES AND JOINTS 


212 

muscular injection of old tuberculin is then given, 0.5 to 
1 milligram according to age, and for the next forty-eight 
hours the patient’s condition is watched, and his tempera¬ 
ture is taken every two hours. A positive reaction is shown 
by a rise of temperature of 2 or 3 degrees Fahr., with an 
increase in the local joint symptoms and a greater or less 
general constitutional reaction. 

Certainty can usually he secured by the guinea-pig test. 
If the joint contain fluid, it may he aspirated, and a cubic 
centimetre or so may be injected into the abdominal cavity 
of the guinea-pig. If no fluid be obtainable, the joint may 
be opened under strict asepsis, and a juece of the synovial 
membrane may be removed, emulsified with a sterile normal 
salt solution, and some of this may be used for the injection. 
The wound should be sutured immediately. The guinea- 
pig is killed in five or six weeks and his viscera are exam¬ 
ined for tuberculosis. A positive guinea-pig test is final. 
A negative test makes tuberculosis improbable in the 
highest degree, so improbable that its presence may 
be discounted. 

Differential Diagnosis. —The chief difficulty lies in 
the differentiation of tuberculosis from the other members 
of the first great type of chronic arthritis. 

Syphilis has its history of initial lesion in the adult, 
and of parental infection in the child, and usually has a 
positive Wassermann and a negative tuberculin reaction. 
The patient may show other signs of syphilis. More than 
one joint is often involved, new periosteal bone may be 
discovered here and there on the shafts, and the skiagram of 
the j oint may show certain peculiarities. Most of the dam¬ 
age in the child is in the epiphysis itself rather than in the 
rnetaphysis, and the epiphysial line may look furred. Some¬ 
times in syphilis there is a marked disproportion between 


JOINT TUBERCULOSIS IN GENERAL 213 

the amount of damage to the bone, as revealed by the 
X-rays, and the joint symptoms. Indeed the bone near 
the j oint may show great rarefaction, and the j oint function 
may be almost perfect. This, when present, practically 
rules out tuberculosis. Sometimes syphilitic joints are 



Fig. 72.—High power photomicrograph of a portion of the rice body shown 

in the preceding figure. 

painless, but not always. Immobilization usually causes 
a marked subsidence of the symptoms in tuberculosis. In 
syphilis it is usually without effect, or may increase the 
discomfort. The most reliable test for syphilis is still 
probably the therapeutic test. Occasionally mercury and 
the iodides will clear up an arthritis supposed to be 
tuberculous. 



214 


INFLAMMATION IN BONES AND JOINTS 


The painful arthritides in young infants, with involve¬ 
ment of the bone in the neighborhood of the joints are never 
tuberculous. They are usually syphilitic or scorbutic. 

Scurvy gives an acute swelling in the region of the 
epiphysial disc, very painful, and extremely sensitive to 
pressure. The child shrieks when it is moved. The dis¬ 
ease occurs most often about the knees, and is usuallv 
multiple. It affects in civilization, artificially fed infants, 
especially those fed on sterilized foods. Other signs of 
scurvy, such as bleeding gums, are usually present. 
Scurvy recovers promptly on a proper diet, coupled with 
the administration of raw fruit juice. 

The arthritides secondary to a diplostreptococcic infec¬ 
tion in the tonsils and the deep urethra are almost always 
multiple, and react to a cleaning up of the original focus. 
Often they show an involvement of the synovial membrane 
out of all proportion to that of the bone, and may lack 
the slow and more or less steady progression of tuber¬ 
culosis. The joints of the fingers are often attacked. 
Abscess formation is practically unknown in them, and 

^ 1 1 e in childi en. Still’s disease is a disease of 

childhood but is multiarticular, and has an enlarged liver 
and spleen and characteristic blood changes. 

Typhoid arthritis is almost always acute, and except in 
the spine, may be painless. 

A differentiation of tuberculous arthritis from that 
of coccidioidal granuloma, is impossible without the detec¬ 
tion of the causal organism; in tuberculosis, the tubercle 
bacillus, in coccidioidal granuloma, the oi’dium coccidioides. 

The differentiation from the second great type of arthri¬ 
tis is comparatively easy. The latter is essentiallv a 

•/ 

disease of middle and late life. The joint creaks and 
grinds, and the obstruction to motion is mechanical; no 


JOINT TUBERCULOSIS IN GENERAL 


21 5 


union is ever present between the articulating bones, except 
in the spine. Examination of the mouth will reveal root 
abscesses about the teeth. The positive diagnosis is made 
with the Rontgen rays. While the bone in both forms 
of arthritis shows rarefaction, the second type is peculiar 
in its ridges of bone at the lines of capsular attachment— 
the so-called lipping and spurring. In addition skiagrams 
of other joints usually show the disease in them, even when 
it is not manifest clinically. Of course, the guinea-pig 
test is negative. 

Traumatic arthritis gives a definite history of a distinct 
trauma immediately precedent to the onset of the disease. 
An arthritis secondary to a capsular tear—a sprain—tends 
slowly to recovery, whereas a fracture is revealed by the 
Rontgen rays. A so-called traumatic arthritis, with a 
negative skiagram, which lasts for any length of time, 
especially one which slowly grows worse, is to be viewed 
with suspicion. Here again the guinea-pig will come to 
our aid. 

New growths .—Benign neoplasms in the joints are 
very rare. It may almost be said that they do not occur. 

Malignant growths .—Carcinomata are always second¬ 
ary, and while observed occasionally in the spine, are rare 
in the joints of the extremities. They affect sometimes 
the marrow of one bone, but do not involve the joint, or 
the other bone of the articulation. A careful search will 
reveal the primary growth elsewhere. 

Sarcoma of bone has no tendency to involve the ioint. 
Sarcoma of the synovial membrane is a great rarity and 
can only be diagnosed by an examination of a piece of the 
tissue under the microscope. 

The so-called giant cell sarcoma, or more properly 
benign giant cell growth, is fairly frequent in the ends of 






216 INFLAMMATION IN BONES AND JOINTS 

the long bones of young adults, especially in the tibia. 
It is encapsulated, circumscribed, covered with a thin shell 
of bone, elastic, crackles like an egg shell, and shows no 
tendency to involve the joint. At operation it bleeds pro¬ 
fusely, and is found to consist of the characteristic more 
or less crumbly granulation tissue, with currant j elly color, 
perhaps with streaks of yellow. A frozen section reveals 
the giant cells and the fibrous tissue, with evidences of old 
hemorrhages. 

Finally a word of caution may be in order. Let it be 
emphasized again that a positive diagnosis cannot be made 

by a clinical examination. This statement may arouse 

%/ 

contradiction, but it is based, not upon theory, but upon 
a mass of evidence. I have in my possession specimens of 
many joints operated on by some of the best men in the 
country. 31 An examination of these specimens, and a 
study of the histories of the patients from whom they were 
taken, shows an astounding proportion of erroneous diag¬ 
noses. Many forms of treatment loudly heralded in the 
past are based upon the unsupported clinical opinion of 
their originators. If, on the other hand we admit our 
nubility arrive at a positive conclusion without the aid 
of the microscope, we are on the road to a correct handling 
of our cases. 

In a general way little can be lost by waiting, before 
proceeding to radical treatment, especially if the joint be 
kept at rest with a splint, and it is far better to remove 
a pair of innocent tonsils from a patient with a tuberculous 
joint, or to give iodides and mercury for a few weeks, than 
it is to resect a joint that is the seat of an inflammation 
secondary to a mild diplostreptococcic infection in the ton¬ 
sil, or to a syphilitic one in the neighboring bone marrow. 

31 Ely, Leonard W.: “Joint tuberculosis.” William Wood and Co., 1911. 





JOINT TUBERCULOSIS IN GENERAL 217 

Prognosis. —This is, generally speaking, good. A 
tuberculous joint, in itself, does not involve the patient s 
constitution, and is without danger unless in the neighbor¬ 
hood of vital structures, as for instance, the joints of the 
spine. Iwo things we fear: first, secondary infection, and, 
second, tuberculosis of other organs. Secondary infection 
immediately makes the prognosis grave, with its attendant 
general septic absorption, and its subsequent amyloid 
disease, and is to be avoided sedulously. The second dan¬ 
ger is in the occurrence of tuberculosis of vital organs. 
The presence of a joint tuberculosis indicates a vulner¬ 
ability to the tubercle bacillus and also the presence of a 
previous focus in the body. Statistics show that a large 
proportion of children with tuberculous joints never reach 
maturity, dying of the results of secondary infection or of 
tuberculosis of the lungs, meninges, etc. 

The various joints carry different percentages of mor¬ 
tality, but modern methods bid fair to change the old 
statistics materially. Formerly spinal tuberculosis in the 
adult was practically invariably fatal. Now it is distinctly 
curable. Perhaps tuberculosis of the sacroiliac joint is 
the most dangerous of all, but this is fortunately rare. 

Treatment. —As in other aspects of the disease, so in 

its treatment, the widest difference of opinion prevails. 

One must have some definite ideas in order to treat a case 

successfully, and, prefacing the subject with the admission 

that the theories and facts I am about to set forth, have not 

been generally accepted, I purpose laying down a very 

definite scheme of treatment. It is based not onlv 

%/ 

upon clinical experience but also upon many years of 
laboratory work. We shall consider other forms of 

*7 

treatment afterward. 



218 INFLAMMATION IN BONES AND JOINTS 

We have seen in our study of the pathology of joint 
tuberculosis, that the uncomplicated disease is strictly con¬ 
fined to the lymphoid marrow, and to the synovial mem¬ 
brane, and that it only attacks other tissues when a second¬ 
ary infection is added. We have seen that tuberculosis 
of the joints is in itself a comparatively harmless disease, 
and only becomes very serious when a pus infection com¬ 
plicates it. We have seen further, not only in our study 
of the pathology, but also in that of the symptomatology, 
that all nature’s efforts at cure seem to be expended in 
the direction of putting the joint at rest. These efforts 
are rarely completely successful, and nature is rarely able 
to effect a cure unaided, after the original marrow tuber¬ 
culosis has spread far enough to involve the joint. Again, 
in the long run, viewed not only with reference to nature’s 
local efforts at cure, but also with reference to her reaction 
to the tuberculous infection elsewhere in the body, it is 
evident that the final outcome depends upon the resistance 
of the ])atient. 

Upon these observations we base our whole manage¬ 
ment of the case, and from them we deduce our three great 
rules of treatment, viz .: 

1. Improve the patient’s nutrition. 

2. Avoid and prevent secondary infection. 

3. Deprive the joint of function. 

Constitutional Treatment. —Under this head would 
come the care of the patient’s teeth and his digestion. He 
should have plenty of good, nutritious food, and the dairy 
from which he gets his milk should be free from suspicion 
of tuberculosis. Diseased tonsils should be removed. 
Occasionally tuberculous nodules will be found in them. 


219 


JOINT TUBERCULOSIS IN GENERAL 

Adenoids also should be removed, on account of their influ¬ 
ence upon the general health. 

The patient should be in the open air as much as pos¬ 
sible. If a child, he should stay out of school, at least for 
a while. Insanitary surroundings must not be tolerated. 
This applies especially to a habitation suspected of infec¬ 
tion from other cases of tuberculosis. 

As to climate, it is hard to speak positively. The 
disease has a wide distribution. A few years ago the sea¬ 
shore was supposed to be specific, now it is more or less 
displaced by the mountains. Rollier, of Leysin, Switzer¬ 
land, has recently called attention again and forcibly to 
the healing powers of sunlight, and maintains that the sun’s 
rays in Leysin possess peculiar therapeutic virtues . 32 The 
patient’s skin is exposed to the direct rays of the sun for 
as much of the twenty-four hours as possible. The expo¬ 
sure is to be begun gradually, the first day one arm for a 
half hour, the second day that arm for an hour and the 
other arm for a half hour, etc. This is continued until 
the patient lies on his frame, or goes about during the entire 
day, with nothing on except a hat and a breech clout. 

While many observers have found that their patients 
do well when exposed to sunlight, no direct action of the 
sun’s rays upon the tubercle bacilli in the bone marrow 
ever has been proved. Laboratory animals might easily 
decide the question. Until such proof is forthcoming we 
shall do well not to abandon local measures. 

Prevention of secondary infection. —All opera¬ 
tions on tuberculous joints, even a simple aspiration, 
must be done with scrupulous asepsis. Every operation 


32 Rollier, Auguste: “Die Heliotherapie der Tuberkulose mit beson- 
derer Beriicksichtigung ihrer chirurgischen Formen.'’ Berlin, J. Springer, 1913. 



220 INFLAMMATION IN BONES AND JOINTS 

must have a definite purpose, and after it the 
wound must be closed. In no circumstances must a path 
be left open between the tuberculous focus and the outside 
air, for we know that infection almost inevitably will be 
established throughout its length. If we attempt to leave 
an exit for the tuberculous material, we shall really provide 
an entrance for pus germs. Tuberculous joints should not 
be scraped and packed. It is folly to insert a curette into 
them and blindly to scrape them out. 

Cold abscesses, if deeply seated, small in size, not 
rapidly growing larger, nor causing severe pressure 
symptoms, may be let alone. Otherwise they should be 
aspirated under strict asepsis, repeatedly if necessary. 
Some surgeons simply apply pressure after the aspiration, 
others inject the abscess cavity with various substances, 
one of the most popular of which is iodoform, in mixtures 
or solution. 

Calot’s formula is olive oil 70 gr., ether 30 gr., creosote 
5 gr., guaiacol 1 gr., and iodoform 10 gr. Two to ten 
grams of this mixture are injected into the abscess, after 
it has been evacuated. A 10 per cent, emulsion of iodo¬ 
form, in glycerin or olive oil, may be tried. 

In aspirating a cold abscess a very large needle or even 
a trocar is necessary. Otherwise the flocculi of broken 
down tissue will clog the needle and stop the flow. The 
aspiration is easier, if the skin and fascia are first slit 
with a scalpel. 

Instead ot aspirating the abscess, some surgeons open 
it freely, empty it, and immediately suture the wound 
carefully. The wisdom of wiping out the cavity is open 
to debate. To scrape its walls, and thereby to cause 
hemorrhage into it, is to invite trouble. 


JOINT TUBERCULOSIS IN GENERAL 221 

LOCAL TREATMENT 

L rom our study ot the anatomy, physiology and path- 
ology ot bones and joints we start our treatment with the 
following facts and theories: 

1. Tuberculosis, when uncomplicated, is strictly a dis¬ 
ease of the synovial membrane and of the lymphoid marrow. 
All the other tissues are immune, or practically so, to the 
direct infection, and suffer simply in the disturbance of 
their nutrition. 

2. If these two tissues disappear, the disease dies out, 
or remains innocuous. It dies out because it has no pabu¬ 
lum, no culture material. It is starved out. 

3. In spite of its subsidence, the tubercle bacilli may 
remain in situ indefinitely, ready at any time to start up 
the disease afresh, if conditions favorable to their growth 

O 

are restored. 

4. The presence of lymphoid marrow and synovial 
membrane in the region of the joint in the adult, is depen¬ 
dent upon function. If function be destroyed these two 
tissues disappear. In children lymphoid marrow exists in 
the shafts as well as in the bone ends, and its presence is 
not affected by function in the joints. 

5. Natures efforts at cure are all directed toward 
destroying the joint function, but unaided she rarely 
accomplishes this completely. 

6. Operations on children’s joints, by their interference 
with the centres of bone growth, cause marked crippling 
and shortening. The general opinion is that even when 
they are carefully done they are not so apt to be curative 
as operations on the joints of adults. 

7. Conservative treatment in children is more likely to 
be followed by a state approaching cure than it is in adults. 
Some surgeons maintain that an actual cure with good 


222 INFLAMMATION IN BONES AND JOINTS 

function can be attained in children by conservative treat¬ 
ment. Others, of which the author is one, consider that a 
cure sometimes can be attained thus, but rarely with any 
painless function. Conservative treatment in both chil¬ 
dren and adults, requires years of careful attention, and is 
almost impossible to carry out to the end in adults. Fur¬ 
ther, there is no absolute way of knowing when the joint 
is well. 

8. No method of eradicating all the tuberculous tissue 
from about the joint has ever been devised, except amputa¬ 
tion of the extremity well above the seat of the disease. 
Amputation, on the other hand, is hardly justifiable. 

9. In spite of the impossibility of removing all the 
tuberculous tissue, we know that resections in the adult, 
when properly performed, are often followed by cure if 
they destroy joint function. On the other hand, no matter 
how much tuberculous tissue may be removed, if function 
remains the disease progresses. 

10. The joints which are easiest to destroy by resection 
are those most easily cured by this means. 

11. It is not absolute immobilization which always is 
responsible for the cure after a resection. When the head 
of the femur is removed, and the stump dislocates upward 
on the dorsum of the ilium, cure often results with a mov¬ 
able femur. 

From these facts and theories we draw our great rule 
for local treatment —Deprive the joint of f unction. 

This rule has two corollaries: 

1. In children the treatment is always conservative. 
Conservative treatment should be followed in them until 
all hope of cure is gone, then amputation should be prac¬ 
tised. No operation should be done which opens up the 


JOINT TUBERCULOSIS IN GENERAL 223 

diseased area. This rule does not apply to ankylosing 
operations on the spine, which are really done on bone at a 
distance from the tuberculous process. 

2. In adults, the treatment is practically always radical, 
and its sole purpose is to destroy permanently all function 
in the joint, and thus to cause such a change in its 
structure as will render it an unsuitable habitation for 
the disease. 

This second rule, it must be said, has not received by 
any means universal acceptance; in fact the great majority 
of surgeons carry out treatment on entirely differ¬ 
ent principles. 

In operating on tuberculous joints the weight of opin¬ 
ion, numerically considered, favors the removal of as much 
tuberculous tissue as possible, and disregards completely 
the idea of destroying the joint. Some surgeons still open 
and pack tuberculous joints, but fortunately this practice 
gradually is losing favor. Some, on the theory of remov¬ 
ing all the infected tissue, advocate amputation in disease 
of the joints of the extremities. While perhaps they may 
seem to follow the logical course, most authorities regard 
the treatment as more radical than necessary. In some 
quarters the practice of scraping out tuberculous joints 
still flourishes. It is mentioned here only to be condemned. 
The details of operative treatment will be taken up under 
the head of the various joints. 

CONSERVATIVE TREATMENT 

Under the head of conservative treatment, many 
expedients have been advocated, and some of these have 
survived. They are employed by many surgeons as adju¬ 
vants, and by some surgeons as their chief means of treat¬ 
ment. Among these may be mentioned passive hyperaania, 


ZU INFLAMMATION IN BONES AND JOINTS 

injections of various sorts, internal medication, external 
applications, tuberculin, the Rontgen rays, etc. 

The method of treatment which has obtained the widest 
recognition, and has established itself more or less generally 
throughout the profession, is that by rest, or in other words, 
by the deprivation of function. To this, in the case of the 
hip and knee, some surgeons add traction to draw the joint 
surfaces apart. 

THE REST TREATMENT 

This is carried out generally in three ways, viz.: By 
recumbency, by metal splints or “braces,” and by plaster 
of Paris dressings, or “casts,” as they are usually but 
erroneously called. The first is useful, especially in the 
spinal disease of children, when reinforced by a 
frame, and to meet special indications in the treatment of 
other joints in children and in adults, as will appear later. 

For the manufacture of braces, a trained brace maker 
is desirable, but by no means essential, if the surgeon knows 
what he wishes to accomplish. It is far better to carry out 
the plan of a simple brace with the aid of the local black¬ 
smith and harness maker, than it is to send a patient to a 
distant brace maker to be furnished with any sort of appara¬ 
tus the latter may choose to supply. Again certain forms of 
braces are more or less standard, and for these the surgeon, 
with a little practice, can take his own measurements, and 
send them to a distant brace maker to be filled. In some 
cases a cast can be made of the limb, and this can be sent 
to the brace maker with directions. 

In the past elaborate and complicated braces were the 
fashion, many of them designed to carry out some idea 
which their inventor considered important, but the modern 
trend is toward simplicity. Having mastered the funda- 


JOINT TUBERCULOSIS IN GENERAL 225 

mental principles of the treatment, a surgeon with a little 
mechanical bent is quite capable of carrying it through. 

In the first place, in the treatment of tuberculous joints, 
apparatus should not he employed to correct deformity. 
The deformity is corrected first and then the apparatus is 
applied, or, especially in the case of the hip joint, the 
apparatus is applied, and then the patient is put to bed and 
traction is made on the apparatus in the line of deformity 
until the deformity is reduced. With plaster of Paris, the 
deformity is partly reduced before the plaster is put on, 
and the correction is continued with each succeeding appli¬ 
cation of plaster. 

With either a brace or a plaster dressing, the deformity 
may be corrected under ether before treatment is begun. 
This is the quickest and in some respects the most satis¬ 
factory method, but it requires great care, on account of 
the danger of stirring up the disease by the manipulation. 
Even then the method is not free from danger, and some 
surgeons refuse to employ it on that account. 

Nothing is to be expected from treatment by braces or 
by plaster in a few weeks, or months. It must be main¬ 
tained continuously for a minimum of one year, and often 
for many years. If a brace gets out of order, it must be 
immediately repaired, and this is one of the disadvantages 
of the brace treatment as compared with that by plaster 
of Paris. Another disadvantage lies in the ability of the 
jmtient to loosen his apparatus. Children will always do 
this if they can. A third disadvantage, and perhaps the 
greatest, unless the surgeon has his own instrument shop, 
is that in a treatment which depends for its success upon 
attention to details, the carrying out of the details is in a 

15 


226 


INFLAMMATION IN BONES AND JOINTS 


large measure not in the surgeon’s hands but in those of 
a mechanic. 

The advantages of braces over plaster are cleanliness 
and the ready accessibility of the joint. 

Plaster of Paris, or one of its substitutes, forms a satis¬ 
factory means of immobilization, if care be used and if 
skill be cultivated in its application. All bony promi¬ 
nences under the dressing must be well padded; muscle 
bellies need no padding. Sheet wadding, the so-called 
interlining, makes a good padding, as does piano felting, 
or silence cloth. Saddler’s felt may be employed, but is 
rather coarse and heavy. A muslin or gauze bandage 
covers the limb, or the limb and part of the trunk, snugly 
and smoothly but not too tightly. The plaster bandages 
are wrung out of warm water, and are evenly applied until 
the dressing is strong enough to withstand the strain to 
which it will be exposed, but not heavy enough to be cum¬ 
bersome. It may be reinforced by extra turns in the 
region of the joints, where the strain comes, or metal or 
thin wooden splints may be incorporated in it. A short 
plaster dressing, reaching a few inches above and below 
the affected joint, is of little use. It shoidd be long enough 
practically to immobilize the joint, and this means, for 
instance, in a joint like the knee, that it should extend 
from the perineum to the malleoli, in the ankle, from the 
toes to the proximal end of the leg, etc. 

If one does a great deal of plaster work one will find 
the so-called stockinette a good material to have on hand 
in various sizes. It is drawn on the part to be bandaged, 
next to the skin. It not only makes the inner surface of 
the dressing smooth, but, if it be cut very long, it can be 


JOINT TUBERCULOSIS IN GENERAL 227 

turned down over the outside of the plaster, and will serve 
to protect the dressing and to keep it clean. The “scratch” 
bandage is a muslin or linen bandage which is slipped under 
the stockinette. It is drawn up and down every day, and 
keeps the skin in good condition, especially if dusting 
powder be liberally used. 

One of the disadvantages of plaster is the fact that it 
may cause pressure sores. Pressure sores are almost 
always the result of improper padding. They make their 
presence known almost immediately by a foul odor, once 
smelled never forgotten, and necessitate the immediate 
removal of the dressing. 

Good plaster bandages can be bought in the shops, 
hut the best are homemade. The knack is easily cultivated. 
Crinoline of a good brand, containing starch but no glue, 
is torn into strips about five yards long. Four and six 
inches are good standard widths. Some surgeons prefer 
unstarched crinoline, some employ gauze. One rubs by 
hand the finest quality of dental plaster into the meshes 
of a strip of crinoline, rolling the bandage loosely mean¬ 
while, and using just as much plaster as the meshes of the 
crinoline will take up, and no more, If each bandage is 
wrapped in paper, and all are kept in a tight tin can, they 
will keep for a long time without deteriorating. 

To apply a plaster dressing one stands a bandage on 
end in a pail about two thirds full of warm water, and 
leaves it there until the bubbles cease to rise. The next 
bandage is then put into the pail, and the first one is re¬ 
moved, wrung out lightly, and applied quickly, smoothly 
and fairly snugly. Reverses are not used. The second 
one is ready when the first one is on. The third one is put 


228 INFLAMMATION IN BONES AND JOINTS 

in the water before the second is taken out. Otherwise 
wet hands scatter drops of water into the pail of plaster 
bandages. If the bandages have been loosely rolled, and 
if a hole have been left down through the centre of each, 
the water permeates the whole quickly, and no delay occurs. 

The dressing extends, as it is put on, well above and 
below the distance intended for the finished dressing, and 
the superfluous portions are cut away afterward with a 
sharp knife. A good knife for this purpose is an ordinary 
pruning knife whose point has been ground away, though 
a jackknife or a potato knife will serve well. A rough 
edge, a wire edge, such as can be put on with a file or a 
coarse stone, is better than a smooth, fine edge. The dress¬ 
ing is best trimmed when it is finished. The trimming is 
accomplished by a combination of tear by a steady pull 
with one hand, and a cut by a stroke of the knife in 
the other. 

If the proper materials have been employed, no salt 
or any other substance is necessary or advisable in the water 
to hasten the setting of the plaster. The dressing should 
be set enough to hold well by the time it is finished. If 
it is not, then something is the matter with the materials 
out of which it is made. Complete setting usually takes 
about 48 hours. Until the end of that time, the dressing 
should be exposed to the air, and should not be subjected 
to undue pressure or strain. 

A good plaster dressing, if not exposed to blows, and 
if kept clean and dry, will last almost indefinitely. The life 
of dressings may be said to be proportional to their cost. 
I have seen them firm and beautiful after a year—in pay 
patients. They are often filthy and soft after a week or 
two, when they have been provided gratis. 



JOINT TUBERCULOSIS IN GENERAL 229 

OTHER NON-OPERATIVE MEASURES 

PASSIVE HYPERiEMIA 33 

This treatment, while by no means new, was revived 
and recommended for joint tuberculosis, by Bier of Ger¬ 
many, and often it is called the Bier treatment on that 
account. It consists in producing a passive congestion in 
a limb, usually by means of an Esmarch bandage. The 
bandage is applied well proximal to the affected joint, 
just tightly enough to make the extremity distal to it 
dusky red and warm, not blue and cold, and is left on at 
first about fifteen minutes daily. The time is gradually 
extended until the bandage remains on two or three hours. 
In cases with abscess special cupping glasses have been 
devised to treat the abscess by suction. Some surgeons 
have had good results with this treatment, in the hands of 
others it has proved a disappointment. 

TREATMENT BY INJECTIONS 34 

The first recommendation of this treatment I have been 
able to find is in an article bv von Mikulicz in 1881. 35 Von 
Mikulicz employed iodoform, and this substance has since 
been employed more widely than any other. Many others 
have also been tried, and some have been loudly praised. 
Among the number may he mentioned hone charcoal, 
iodin, phenol, arsenious acid and corrosive sublimate, 

33 Bier, A.: “ Ueber ein neues Verfahren cler conservativen Behandlung 
von Gelentuberkulose.” Ver. d. deut. Gesell. f. Chir., 1892, i, 91. 

Bier, A.: “ Hyperaemie als Heilmittel.” Leipzig, F. C. W. Vogel, 1907. 

Ely, Leonard W. : “ The Bier treatment in tuberculous joint disease.” 
Surg., Gyn. Obst., 1910, x. 63 (bibliography). 

34 Ely, Leonard W.: “The injection treatment of tuberculous joints.” 
J. Am. Med. Ass., 1913, lxi, 1453. 

35 Von Mikulicz: “Ueber das Iodoform als Verbandmittel bei Knochen- 
und Gelenktuberculose.” Berliner klin. Woch., 1881, xviii, 230. 



230 


INFLAMMATION IN BONES AND JOINTS 


acidulated solution of calcium sulphate, zinc chloride, bal¬ 
sam of Peru, naphthol camphor, and formaldehyde solu¬ 
tion. Some of these substances are by nature germicidal, 
but others are not. The surgeon who would try the treat¬ 
ment of tuberculous joints by injection should assure him¬ 
self that the substance to be injected is at least sterile. 
Iodoform may be used in a 1-10 solution in ether, or 
as an emulsion. 

Beckys Paste .'* 1 —This paste, consisting of bismuth 
subnitrate 1 part and vaseline 2 parts, sometimes with 
white wax added, has had quite a vogue, especially in cases 
with infected sinuses. The treatment has caused several 
deaths from bismuth poisoning, and should be employed 
with great circumspection. Beck emphasizes the danger 
of using it in the presence of a sequestrum. In the effort 
to gain the mechanical effect of the paste without the dan¬ 
gers of the bismuth ingredient other surgeons have recom¬ 
mended substitutes. While it is doubtful that any of these 
pastes have a specific effect upon the tubercle bacilli, it is 
possible that they act mechanically to check the secondary 
infection, and so convert the disease into a simple, uncom¬ 
plicated joint tuberculosis. 

TUBERCULIN TREATMENT 

This treatment was quite popular a few years ago, and 
is still advocated by some surgeons, especially when com¬ 
bined with other measures, such as rest. 

THE RONTGEN RAYS 

Theoretically this should be an almost ideal form of 
treatment, on account of the action of the rays upon lvm- 
phoid tissue. Practically the results of treatment have not 

30 Beck, Emil G.: “ Bismuth paste in chronic suppurations.” St. Louis. 
C. V. Mosby. Co., 1915. 





JOINT TUBERCULOSIS IN GENERAL 


231 


justified the expectations that were entertained of it. Per¬ 
haps increasing knowledge of this therapeutic agent may 
teach a way to employ it more successfully. 

BIBLIOGRAPHY 

Allison, Nathaniel: “Tuberculosis of bone, results of a study.” Arch, of 
Surg., 1921, ii, 593. 

Batzner, W.: “ Zur Trypsinbehandlung der chirurgisclien Tuberkulose.” Arch, 
f. klin. Chir., 1911, xcv, 89. 

Blanchard: “Bismuth paste.” Med. Rec., 1912, lxxxi, 941. 

Bocker, W.: “ Ueber die berdform'ig Tuberkulose der Extremitatenknochen.” 
Deut. med. Woch., 1912, xxxviii, 2117. 

Brandes and Matt, C.: “ Tuberkelbazillen im stromenden Blute bei chirurgisclien 
Tuberculose.” Revue de la Tuherculose, 1911. 

Broca, Aug.: “ Osteo-arthritis tuberculeuses precedes de typho-bacillose. 
Tuberculose osseuse a foyers multiples.” Revue de la Tuberculose, 1911, 
vm, 1. 

Brown, Edward M.: “Tuberculosis of bones and joints.” N. Y. Med. Jour., 
1910, xcii, 905. 

Cadbury, William W.: “Tuberculosis of the bones and joints.” Henry Phipps 
Institute, Report, 1906-1907, iv, 203. 

Campbell, Willis C.: “An analysis of 51 bone and joint affections treated 
by heliotherapy, with special reference to tuberculosis.” Am. Jour. 
Orth. Surg., 1917, xv, 1. 

Chalier, Andre et Maurin, A.: “ Sur une forme benigne de pyarthrose 
tuberculeuse primitive sans lesions osseuses.” Revue d’Orth., 1913, lv, 41. 

Cheyne, W. Watson: “Professor A. E. Wright's method of treating tuber¬ 
culosis.” Lancet, 1906, i, 78. 

Duchinoff: “Ueber den Uachweis von Tuberkelbacillin, etc.” Beit, z klin. 
Chir., 1912, lxxix, 1. 

Eastwood, Arthur and Griffith, Fred: “The characteristics of tubercle 
bacilli in human bone and joint tuberculosis.” Jour. Hygiene, 1915-1917, 
xv, 257. 

Forssell, Gosta: “A few notes on the diagnosis and differential diagnosis of 
tuberculosis in bones and joints.” Arch. Radiology and Electrotherapy, 
1912, xxv, 257. 

Fraser: “Pathology of bone tuberculosis.” Path, and Bacteriology, 1912, 
xvii, 254. 

Fraser, John: “ Observation on the situation of the lesions in osseous tubercle. 
Edinburgh Med. Jour., 1912, ix, 436. 

Fraser, John: “The relative prevalence of human and bovine types of tubercle 
bacilli in bone and joint tuberculosis occurring in children.” Jour. Exper. 
Med., 1912, xvi, 432. 


232 INFLAMMATION IN BONES AND JOINTS 

a 

Fraser, John: “An experimental study of bone and joint tuberculosis.” 
Jour. Exper. Med., 1913, xvii, 364. 

Freund, Leopold: “The treatment of tubercular osteo-arthritis by Rontgen 
ray.” Arch. Rontgen Ray, 1908-1909, xiii, 89. 

Friedlander: “Die tuberkulose Osteomyelitis der Diaphysen langer Rohren- 
knochen.” Dent. Zeit. f. Chir., 1904, lxxiii, 249. 

Friedrich: “ Experimentelle Beitriige zur Kenntniss der chirurgischen Tuber¬ 
kulose.” Rent. Zeit. f. Chir., 1899, liii, 512. 

Garre, C.: “Die behandlung der Knochen und Gelenktuberkulose.” Arch. f. 
klin. Chir., 1913, ci, 376. 

Gauvain, H. J.: “A comparative study of the reactions to human and bovine 
tuberculin applied by the method of von Pirquet.” Lancet, 1917, ii, 519. 

Honsell, B.: “ Ueber Trauma und Gelenktuberkulose.” Beit. z. klin Chir., 
1900, xxviii, 659. 

Jansen, M.: “Die polyarticularen Muskeln als Ursache der arthrogenen 
Contracturen.” Arch. f. Klin. Chir., 1911, xcvi, 616. 

Kleinberg, S.: “Tuberculin, its use in the treatment of bone and joint 
tuberculosis.” Jour. Orth. Surg., 1919, i, 722. 

Koenig, F.: “Die specielle Tuberculose der Knochen und Gelenke.” Berlin, 
August Hirschwald, 1896. 

Kiscii, Eugen: “ Diagnostik und Therapie der Knochen und Gelenktuber¬ 
kulose.” Leipzig, T. C. W. Vogel, 1921. 

Koenig, Fr. : “Die Tuberculose der Knochen und Gelenke.” Berlin, August 
Hirschwald, 1884. 

Krause, Fedor: “Die Tuberkulose der Knochen und Gelenke.” Deut. Chir., 
1899, xxviii. 

Kuttner: “Die Osteomyelitis tuberkulose des Schaftes langer Rohrenknochen.” 
Beit, z klin. Chir., 1899, xxiv. 449. 

Lexer, E.: “ Die Entstehung entziindliclier Knoclienherde und ihre Beziehung 
zu den Arterienverzweigungen der Knochen.” Arch. f. klin. Chir., 1903, 
lxxi, 1. 

Marciiard: “ Traitement des cavites tuberculeuses osteo-articulaires par 
le procede de Mosetig.” Revue med. Suisse Romande, 1912, xxxii, 797. 

Melchior: “ Ueber symmetrische Diaphysen-tuberkulose.” Berliner klin. Woch., 
1913, 1, 513. 

Nieiians: “Die Rolle der isolierten Muskelatrophie als diagnostisches Symptom 
zur Lokalisation von tuberkulosen Knoclienherden.” Zentralhlatt f. Chir., 
1910, xxxvii, 852. 

Orberst, Adolf: “ Die herdformige Tuberkulose der grossen Extremitiiten- 
knochen, mit besonderer Beriicksichtigung der metaphysiiren Lokalisation.” 
Deut. Zeit. f. Chir., 1913, cxxiv, 431. 

Schuller, Max: “ Gelenkleiden.” Stuttgart, Ferdinand Enke, 1880. 


JOINT TUBERCULOSIS IN GENERAL 233 

Stiles, Harold, J.: “Major operations on children’s joints.” Brit. Med Jour 
1912, ii, 1356. 

Todd, T. Wingate: “The end result of excision of the elbow for tuberculosis.” 
Ann. Surg., 1913, lvii, 431. 

Twinch, S. A.: “ The rational treatment of bone and joint tuberculosis.” 
Am. Jour. Ortli. Surg., 1918, xvi, 295. 

Vignard, ET Mouriquand, E.: “ Tuberculose diaphysaire spina ventosa des 
grands os longs.” Revue d’orthopedie, 1908, ix, 481. 

Willard, De Forest and Thomas, B. A.: “Therapy by bacterins and tuber¬ 
culins in mixed suppurative bone and joint disease.” Ann. Surg. 1910, 
li, 761. 




















, 

































































































































SECTION V. 


TUBERCULOSIS OF SPECIAL JOINTS 







CHAPTER I. 


TUBERCULOSIS OF THE SPINE, POTT’S DISEASE 

The disease affects primarily, principally, and almost 
invariably, the marrow of the vertebral bodies. The pedi¬ 
cles, laminae and lateral masses, composed as they are of 
dense hone, escape. The lateral articulations seldom if 
ever are involved. The starting point seems usually to he 
near the anterior portion of the body. The disease may 
he confined to one vertebra, hut usually attacks several, 
spreading from one to the other beneath the anterior liga¬ 
ment. The intervertebral disc probably escapes until the 
hone in its immediate vicinity is damaged. The whole body 
may he attacked, or its anterior portion exclusively. 
Sometimes the process involves the anterior part of several 
vertebra?, leaving the rest unaffected. 

As the marrow of the bodies becomes more and more 
involved, the hone is killed, the body softens, and then 
collapses slowly, at first in its anterior portion, thus taking 
on the shape of a wedge with the point forward. Later 
the entire body may be destroyed. As the body collapses, 
the superimposed weight is transferred to the lateral 
masses, and in extreme cases perhaps even to the spinous 
processes and laminae. As this takes place, the spine above 
the lesion slowly falls forward, causing a protrusion back¬ 
ward of the spinous processes at the site of the disease— 
the well-known kyphosis, buckle or hump. At first, this 
kyphosis is almost invariably angular, but in the later 
•stages of the disease it tends to become rounded. 

The vertebras, becoming involved one after another, 
soften and collapse, the weight of the trunk above bending 

237 



238 


INFLAMMATION IN BONES AND JOINTS 


the spine more and more forward to fill in the space left 
by their destruction. This causes a steady growth in the 
angular kyphosis, accelerated in the thoracic region by the 



Fig. 73. —Posterior aspect of tuberculous spine 
of child, upon which a Hibbs operation was 
done. The symptoms persisted, and at a later 
operation a bone graft was laid down on the 
laminae. The patient died three months later 
of tuberculous meningitis. 

tion of least resistance. 


normal kyphosis there, 
retarded in the lumbar region 
by the normal lumbar lordo¬ 
sis. Spontaneous cure may 
be effected at length by an 
ankylosis of the spinous proc¬ 
esses after an enormous 

amount of deformity has 

•/ 

taken place, but a complete 
fusion is probably very rare. 
Occasionally at operation on 
old cases, however, evidences 
of bony union here and there 
are unearthed. 

As the bodies collapse, the 
necrotic material is squeezed 
out anteriorly, and collects 
under the anterior ligament 
as a fusiform mass visible in 
the Rontgen plate. It may 
remain there indefinitelv as 
a cold abscess, or at any 
time it may rupture the 
anterior ligament, and start 
on its journey to the sur¬ 
face, its course determined 
by gravity and the direc- 
n high cervical disease it 


appears in the back of the throat as a post-pharvn- 
geal abscess; in disease lower down, as a fluctuating 




TUBERCULOSIS OF THE SPINE 239 

swelling at the side ot the neck. In thoracic disease the 
abscess lies at first in the posterior mediastinum, then, 



Fig. 74.—Spine shown in preceding figure, laid open from behind. Note the wedge shape of the vertebra 
first involved. Note also that although the two vertebrae above are extensively involved, they have 
been kept from collapsing by the bony bridge in the laminae 

making its way behind the diaphragm, it gains the sheath 
of the psoas muscle, and, following this downward under 



240 


INFLAMMATION IN BONES AND JOINTS 


Poupart’s ligament, comes through the saphenous opening, 
and appears finally as a fluctuating swelling on the antero¬ 
medial aspect of the thigh. In rare instances a cold ab¬ 
scess makes its way through Petit’s triangle, and appears 
in the back. 

The tuberculous material is squeezed out not only 


Fig. 75.—Tuberculosis of the spine. Photo¬ 
graph of the stained slide, sagittal section. 

The child died five months after a Hibbs 
operation, from an intercurrent disease. Bony 
union of spinous processes at A. Note wedge 
shape of affected vertebra, with apex forward, 
and the indication of the beginning of a cold 
abscess anteriorly. When one looks at the 
mass of tuberculous granulations on the pos¬ 
terior surface of the body of the vertebra, 
pushing out into the spinal canal, one can 
readily understand the pathogenesis of Pott’s 
paraplegia. The marked calcification in the 
diseased vertebra shows that healing was 
in progress. 

anteriorly, but also posteriorly, where it accumulates be¬ 
tween the vertebral body and the dura. If it attain pro¬ 
portions great enough, it exerts pressure upon the anterior 
columns of the cord, and causes paralysis in the parts 
below the lesion, the so-called Pott’s paraplegia. Even in 








TUBERCULOSIS OF THE SPINE 


241 


cases with marked deformity it is doubtful if this paralysis 
ever is caused by bony pressure. It is most frequent in 
cervical disease. When the cold abscess breaks through 
the spinal membrane it causes a tuberculous meningitis. 1 

In spite of extensive destruction of bone, the spinal 
foramina are not compromised in their lumen. Pressure 
upon the spinal nerves as they pass through them probably 
never occurs. 

In high cervical disease dislocation may take place, 
with instant death from damage to the phrenic nerve. In 
thoracic and in lumbar disease with much deformity, the 
viscera are distorted, displaced, and often compromised in 
their function. Whether from this cause or not, there is a 
peculiar facies of old hunchbacks that can be recognized 
at a glance. The neck is short, the shoulders are broad, 
the arms appear abnormally long, and the trunk is short. 
This last factor accentuates the diminutive size of these 
hunchbacks when they sit down. 

SYMPTOMATOLOGY 

Pain is usually the most pronounced symptom. It 
varies in intensity from a slight feeling of discomfort or 
stiffness to great severity. It may be more or less constant, 
or it may intermit. Frequently it comes in paroxysms, 
especially in a child. Evidently as the result of an un¬ 
guarded movement the child suddenly doubles up, scream¬ 
ing with pain. In the early stages of the disease the pain 
is more in the nature of a feeling of stiffness, noticed for a 
while in the morning after rising, and wearing away with 
exercise. This also occurs especially in the child, and is 
temporary. The pain of a tuberculous joint is almost 
always aggravated by motion. 

1 Ziegler, Ernst: “ Lehrbuch der speziellen pathologischen Anatomie/ 
11th. Auflage. Jena. Verlage von Gustav Fischer, 1906, Band ii, Seite 371. 


16 




242 


INFLAMMATION IN BONES AND JOINTS 


The pain may be located in the back, at or near the 
lesion, or at a distance from it. At some period of the 
disease pain in the back will be experienced, but it may 
be insignificant in comparison with that felt out along the 
course of the spinal nerves—the so-called referred pain 
of Pott’s disease. This pain varies of course according 
to the location of the disease. In the cervical spine it may 
be felt in the neck, or in the arms as a brachial neuralgia, a 
“neuritis.” In the thoracic spine it radiates around the 
trunk as an intercostal neuralgia, or “muscular rheuma¬ 
tism.” In disease of this region the patient often exhibits 
a peculiar grunting respiration, or a futile spasmodic cough. 

In low thoracic or in lumbar disease a typical “girdle 
pain” may be present. In lumbar involvement the patient 
may complain of pain along the anterior crural or the 
sciatic nerve. In adults a persistent sciatica, often double, 
may for months be the only sign of trouble. In women the 
pain in the back and in the abdomen may be mistaken for 
that of a uterine displacement or perineal laceration, and, 
in either sex, for that of an appendicitis. 

These so-called referred pains are usually ascribed to 
irritation of the spinal nerves as they pass through the 
spinal foramina, but we have seen that this cannot be so, 
for the foramina remain patent and unchanged. The pain 
is a true referred pain, similar to that occasionally experi¬ 
enced in the foot after it has been amputated, or in the knee 
with hip joint disease. It does not differ essentially from 
the referred pains of tabes. When a painful stimulus 
comes in over a nerve from an inflamed spinal joint, it is 
referred to the paths over which painful stimuli usually 
come in at that level. 

The muscular spasm which is so characteristic of the 
. disease holds the joints of the spine more or less at rest. 


TUBERCULOSIS OF THE SPINE 


£43 


When it relaxes in sleep, the joint moves, and the child 
wakes with a cry—the so-called night cry, heard more often 
with Potts disease than with disease of the other joints. 
When the mother reaches the child’s bed she often finds 
it asleep. 

The muscular spasm is responsible also not only for the 
feeling of stiffness of which the patient complains, but also 
for the very evident appearance of stiffness which he pre¬ 
sents, and for the limitation of motion of a greater or 
smaller segment of the spine. This is nature’s involuntary 
protective mechanism, and it is soon reinforced by the 
voluntary efforts of the patient. He holds himself stiffly, 
and avoids j ars. Often he adopts an attitude almost charac¬ 
teristic of disease of a certain part of the spine. Thus in 
high cervical disease, the head may be acutely flexed, bring¬ 
ing the chin down on the sternum. When the disease is 
somewhat lower the head may be thrown forward or back, 
or it may be tilted to the side in one of a number of different 
attitudes. In thoracic disease the shoulders may have an 
exaggerated appearance of squareness. In lumbar disease 
the trunk is held in superextension, and the abdomen is 
protruded. Both in thoracic and in lumbar disease the 
patient, especially if he be a child, will often support him¬ 
self with his hands while sitting. 

It is seen therefore that there is nothing characteristic 
of the attitude of a tuberculous spine, but that it varies with 
the region involved, and may be described simply as a 
departure from the normal. 

Muscular spasm causes also limitation of motion, usu¬ 
ally more marked in flexion than in extension. Muscular 
spasm and limitation of motion really go hand in hand. 
Each mav be said to cause the other. The limitation is 
not general, but affects that portion of the back where the 


244 


INFLAMMATION IN BONES AND JOINTS 


disease is located. It is very rarely absent, but is some¬ 
what harder to detect in the thoracic than in the cervical 
or lumbar spine. To elicit it, one directs the patient to 
put the various regions of the spine through their normal 
range of motion, and notes any restriction. 

In the examination of the cervical spine one should 
hear in mind that nodding of the head takes place at the 
occipito-atlantoid articulation, rotation at the atlanto- 
axoid, and flexion, extension and lateral motion in the 
other cervical articulations. In disease of the lumbar 
spine, when the patient is directed to pick up an object 
from the floor, he will not bend forward naturally, with 
a flexed spine, but, with his trunk held rigidly upright, he 
will flex his hips and his knees, and pick the object up at 
his side. Each region has its peculiar stiffness, hut 
wherever the lesion may be, the muscular spasm is 
responsible for a general appearance of stiffness and awk¬ 
wardness, often to he easily noticed as the patient moves 
about. Cases of Pott’s disease without limitation of mo¬ 
tion are very rare, but they do occur. 

The characteristic deformity of Pott’s disease is a 
kyphosis, a curve or angulation with posterior convexity. 
It is wont to appear earlier, and to he more noticeable in 
the thoracic region, where the spine has a normal backward 
convexity, than in the lumbar, where the convexity is for¬ 
ward. It usually appears earlier in children than in adults. 
In the lumbar spine of the adult it may be absent indefi¬ 
nitely. At first it is distinctly angulated—a knuckle—hut 
later, with the involvement of several vertebra?, it becomes 
rounded off. On the other hand, in adults, the kyphosis 
may he rounded from the start, and in the thoracic region 
may constitute simply an exaggeration of the normal tho¬ 
racic curve. In early lumbar disease the kyphosis may he 




TUBERCULOSIS OF THE SPINE 


245 


represented by a flattening, 
which replaces the normal 
lumbar lordosis. 

A lateral curvature may 
be added to the kyphosis, or, 
occasionally, and less often 
in children than in adults, it 
may be the first deformity 
to appear. It is said to be 
caused by the greater in¬ 
volvement of one side of the 
column, or to disease in a 
lateral articulation. 

Above and below the 
knuckle in early cases, the 
spine is usually flattened. 

Generally speaking, a 
change in the curve in any 
region of the spine must be 
compensated by change in 
contour of other regions, 
and in old case of Pott’s 
disease with marked kypho¬ 
sis, lordosis, equal or nearly 
equal will be present else¬ 
where, 

deformity. This compensa¬ 
tory lordosis helps to differentiate spinal tuberculosis 
from other forms of spinal arthritis. In these it is 
usually not present. 

Cold abscess formation is very frequent in spinal tuber¬ 
culosis, but on account of its distance from the surface, 





accentuating the Fig. 76. —Tuberculosis of the cervico-thoracic 
° spine, treated intermittently with jackets for 

nine years. 


246 


INFLAMMATION IN BONES AND JOINTS 


the abscess, if of small size often escapes recognition. It 
need cause no symptoms whatever. If it increase in size, it 

may cause pressure 
symptoms upon 
contiguous struc¬ 
tures. An abscess 
in the cervical re¬ 
gion may give rise 
to dysphagia, or to 
dyspnoea. When 
it comes from the 
upper part of the 
cervical spine, it is 
recognized as a 
fluctuating swell¬ 
ing in the posterior 
pharyngeal wall. 
Lower down it 
may appear as a 
fluctuating swell¬ 
ing in the side of 
the neck. 

A cold abscess 
in the thoracic re¬ 
gion is hard to 
detect clinically, 
but in the lumbar 
region it may be 
palpated as 
a deeply seated, 
tense, obscurely 
fluctuating mass in the flank, lying on or in the sheath of 
the psoas muscle. The irritation of its presence causes 



Fig." 77. —Tuberculosis of the lumbar spine. Albee operation. 
The patient was unruly after the operation, and the disease 

was not arrested. 


TUBERCULOSIS OF THE SPINE 


247 


a spasm and a contraction of the psoas-iliacus muscle, 
recognized clinically by the fixed flexion deformity of the 
hip. If the patient contin¬ 
ues to be about on bis feet, 
the abscess follows along 
down the sheath of the mus¬ 
cle, becoming more and 
more superficial, passes 
under Poupart’s ligament, 
and usually points on the 
antero-medial aspect of the 
thigh in the region of the 
saphenous opening. In 
exceptional cases it may 
pass through Petit’s trian¬ 
gle, and point in the back, 
or through the sciatic fora¬ 
men, and appear in the 
gluteal region. 

When these cold abscesses 
become infected secondarily 
by pus germs, constitutional 
symptoms of septic absorp¬ 
tion supervene, and a condi¬ 
tion of chronic suppuration 
results, if the patient survive 
the acute stages, which may 

run OI1 indefinitely. W e can p IG yg.—Tuberculosis of the second lumbar 
. . n ££ • vertebra. Guinea pig test with contents of psoas 

picture the State Ot an airs, abscess was positive. Hibb’s operation in Sep¬ 
tember, 1920; photograph taken nineteen months 

in such a case, and cannot later> Note absence of deformity. 

expect healing. At the bottom of a long, narrow and tor¬ 
tuous sinus, is a secondarily infected tuberculous bone 



248 


INFLAMMATION IN BONES AND JOINTS 


cavity, perhaps containing sequestra. Healing in such 
circumstances is highly improbable, unless we can obliter¬ 
ate the cavity, and remove the sequestra. 

Pott’s paraplegia is a compression myelitis caused by 
pressure on the anterior columns of the cord by the tuber¬ 
culous inflammatory products beneath the posterior com¬ 
mon ligament, seldom if ever by bony pressure. It is most 
often seen in disease of the cervical or of the upper thoracic 
spine. It is a spastic paralysis, affecting usually the lower 
extremities. It begins as a slight unsteadiness in walking, 
and sometimes progresses to complete motor paralysis. 
The knee jerks are increased, unless their centre in the 
cord be affected, when they may be absent. Ankle clonus 
is usually present. In severe cases the sphincters of the 
bladder and of the rectum may be involved, with resulting 
incontinence of urine and of feces. Motion is affected 
much more than sensation, but anaesthesias or paresthesias 
may be present. 

In mild cases, properly treated, the paralysis may clear 
up in a short time, but usually it lasts for months. Occa¬ 
sionally it may be permanent. Sometimes a spastic para¬ 
plegia is the first thing to draw attention to the presence 
of a tuberculous lesion of the spine of an adult, and on the 

cases of Pott’s paraplegia have been 
mistaken for essential cord lesions, with no thought for 
the bone lesion underlying them . 2 

DIAGNOSIS 

This is made tentatively, in early cases, on the symp¬ 
toms and physical signs, and confirmed by the Rontgen 
picture. The patient complains of pain and stiffness, 
usually of gradual onset and of some duration. In a child 

“Painter, Charles F., and Moore, George C.: “Pott’s paraplegia.” Am. 

J. Orth. Surg., 1910-11, viii. 306. 



TUBERCULOSIS OF THE SPINE 


249 


the trouble may have come on after an attack of measles, 
whooping cough, or scarlet fever. Examination shows 
a peculiar attitude, with a change in contour of the spine, 
usually in the shape of an angular kyphosis. Muscular 
spasm and limitation can be demonstrated by attempting 
to put the spine through its normal range of motion. 
Often a deep abscess can be palpated. The knee jerks 
may be changed. A positive test with old tuberculin may 
he of assistance. 

The X-rays show a rarefaction of the vertebral body, 
usually with some compression, and a diminution of the 
space between the bodies. 

DIFFERENTIAL DIAGNOSIS 

From coccidioidal granuloma, the differentiation is im¬ 
possible without the examination of some of the diseased 
tissue. The other members of the first great type which 
are most important to differentiate, are syphilitic arthritis, 
typhoid arthritis, and the arthritis caused probably by 
diplostreptococcic infection, supposed to be due to chronic 
infection in the tonsil or in the deep urethra. 

Syphilitic arthritis in the spine is rather rare, doubly 
so in children. As a rule, a history of syphilis can be 
elicited, with a positive Wassermann test, and other signs 
of syphilis can be found. Muscular spasm, and limitation 
of motion are not so marked, the deformity is usually less, 
and the distinct kyphosis, the evidence of a crushed verte¬ 
bra, is lacking. The wedge shaped crushing therefore is 
lacking in the X-ray plate also. Antisyphilitic treatment 
causes an improvement of the disease. 

Typhoid spine is much more acute in its onset than 
tuberculosis, and occurs in the late stages of typhoid fever 
or during convalescence. The pain, stiffness and muscular 


&50 INFLAMMATION IN BONES AND JOINTS 

spasm are out of all proportion to the bony damage as 
revealed by deformity or the X-ray. A kyphosis is ex¬ 
tremely rare in typhoid spine, and the Rontgen rays show 
little if any rarefaction. A bony ankylosis of two vertebrae 
makes one suspect typhoid spine. 

In the chronic spinal arthritis caused by an infection in 
the tonsil or in the deep urethra, the involvement is not 
circumscribed as in tuberculosis, but more or less general. 
Often the entire spine, with the exception of the two upper¬ 
most joints, is affected. For some reason these usually 
escape. The affection seems to be largely in the soft parts 
of the joints; the stiffness and pain are wont to be out 
of all proportion to the damage in the bone. The X-rays 
do not show the extensive local destruction of bone, with 
the compression and coalescence of the vertebral bodies. 
Cold abscess formation does not occur in this form of 
arthritis, and a local kyphosis does not form. 

In the second great type of spinal arthritis the stiffness 
and limitation may be more or less localized, and a slight 
angular kyphosis might possibly give rise to a suspicion 
of tuberculosis. Usually however there is no abnormal 
kyphosis, and the disease is more or less general in the 
spine, even though it may be more pronounced in a 
certain segment. The second type of chronic arthritis 

in middle aged or elderly persons. The 
two diseases can be differentiated absolutely by the 
Rontgen rays. Spurring and lipping are present in 
the second type of chronic arthritis and are absent in 
tuberculosis. 

Spinal fractures cause an angular deformity similar 
to that of Pott s disease. The diagnosis is to be made 
upon the distinct history of trauma followed immediatelv 
by the deformity and by other symptoms, especially by 


TUBERCULOSIS OF THE SPINE 


251 


symptoms of cord pressure such as incontinence of fasces 
and urine. Before the injury there must have been no 
symptoms referable to the spine. The Rontgen rays show 
crushing and distortion, often a broadening out of the 
body, rather than a rarefaction. 

In torticollis such motions as put the muscles involved, 
usually the sterno-mastoid and trapezius upon the stretch, 
will be painful and limited, and the deformity will be 
typical of their contraction, whereas in tuberculosis of 
the cervical spine the muscular spasm and limitation of 
motion will be more general. Torticollis following trauma, 
is sometimes caused by a fracture of one of the cervical 
vertebras, and can be detected by the Rontgen rays. 

Rot ary-lateral curvature is accompanied by little pain, 
if any. Severe ca^es may cause an ache or a tired feeling 
in the back. Lateral curvature is a postural deformity, 
not a disease; hence subjective symptoms will be slight or 
absent. The curve is not only lateral, but it has a twist 
also which throws the ribs into prominence on one side 
of the back (best seen when the patient leans forward) 
and makes one shoulder high or one hip prominent. The 
curve is often S-shaped. No knuckle or kyphosis is ever 
present on the spine, nor can muscular spasm be detected. 
The apex of the deformity is always on the ribs—also best 
seen when the patient bends forward. 

Rickets .—In a young child with severe rickets, the 
continuous sitting posture necessitated by his weakness 
causes a long posterior curve, often with more or less 
angularity in the thoracic region. This curve may be some¬ 
what fixed, but as a rule, if the child be laid prone, his 
hips be raised from the table, and the kyphosis be pressed 
in with the palm of the hand, the curve can be obliterated, 
or almost so. In addition, the child will present other 



252 


INFLAMMATION IN BONES AND JOINTS 


evidences of rickets. For some unknown reason, the com¬ 
bination of rickets and joint tuberculosis in the same pa¬ 
tient, is extremely rare, if it ever occurs. 

Sarcoma is more rapid in its course than tuberculosis, 
and causes a more diffuse, rounded, irregular deformity, 
not following the spinous processes, and sometimes sensi¬ 
tive to pressure. The Rontgen rays may show extensive 
destruction of bone, possibly combined with the formation 
of new bone. Sarcoma is very rare. 

Carcinoma occurs as a metastasis of a growth elsewhere, 
and is accompanied by agonizing pain not relieved by rest. 
The Rontgen rays show an extensive destruction of the 
vertebral bodies but without the coalescence and wedge 
shape of tuberculosis. Careful search reveals the pri¬ 
mary growth. 

Hip disease is sometimes confused with the psoas con¬ 
traction of Pott’s disease. In the former all motions of 
the joint are limited, whereas in psoas contraction, if the 
psoas-iliacus be relaxed by further flexion of the thigh, 
the motions of the hip are free. 

Persistent “lumbago” and “sciatica” are to be viewed 
with suspicion until the absence of a bony lesion has been 
demonstrated. 


PROGNOSIS 

Until recently, the prognosis in tuberculosis of the 
spine was bad, but modern methods of treatment have 
changed the outlook. Prognosis in simple Pott’s disease 
now is good. Abscess formation makes the prognosis 
unfavorable. Disease of the cervical region, on account of 
the proximity of vital structures has an added danger. 
Under operative treatment Pott’s disease can be brought 
to a standstill within six months. Without operation three 


TUBERCULOSIS OF THE SPINE 


253 


years may be said to be the minimum duration of treatment. 
Bony deformity once present, is permanent. Perhaps by 
strict attention to details and by vigorous measures, the 
hump may sometimes be made a trifle smaller. Under 
modern methods of treatment, the enormous humps, so 
frequently seen in former days, are growing rarer. 

TREATMENT 

The treatment of tuberculosis of the spine consists in 
immobilization, and this immobilization may be made com¬ 
plete, by operation, or relative, by apparatus. Realizing 
the importance of rest in the treatment of this disease many 
surgeons had attempted to devise an operation which would 
completely ankylose the spine at the seat of the disease. 
Hibbs 8 ’ 3 4 ’ 5 6 7 8 was the first to solve the problem, getting his idea 
from the occasional cure wrought by nature through the 
fusion of the spinous processes. Albee followed Hibbs 
shortly. 0, ' 8 Various modifications have been made of these 
two operations, but they remain standard. Enough time 
has not elapsed for a final opinion as to their merits. Some 
surgeons refuse to employ them, and cling to the treatment 
by apparatus. Others, of whom the author is one, consider 
that they have practically displaced the old treatme nt, and 
employ them on every possible occasion. Other s pursue 

3 Hibbs, R. A.: “An operation for progressive spinal deformities.” N. Y. 
Med. J., 1911, xciii, 1013. 

4 Hibbs, R. A.: “Operation for Pott’s disease of the spine.” J. A. Med. 
Ass., 1912, lix, 433. 

c Hibbs, R. A.: “ Treatment of vertebral tuberculosis by fusion operation.” 
J. A. M. A., 1918, Ixxi, 1372. 

6 Albee, F. H.: “Bone transplantation etc., in Pott’s disease.” N. Y. Med. 
Jour., 1912, xcv, 469. 

7 Albee, F. H.: “A study of 539 cases of Pott’s disease, etc.” Am. J. Orth. 
Surg., 1916, xiv, 134. 

8 Albee, F. H.: “Transplantation of a portion of the tibia into the spine 
for Pott’s disease.” Journ. of the A. Med. Ass., 1911, lvii, 885. 



254 


INFLAMMATION IN BONES AND JOINTS 



a middle course. Each operation has its merits. The 
Albee is much the easier to perform, but the Hibbs seems 
much the more reliable and secure. Both are serious 

operations, and should 
never be performed 
without the assistance 
of a skilled anaesthetist . 9 

The Hibb's Opera¬ 
tion.— The patient lies 
prone, with pillows so 
disposed under his 
chest and shoulders, that 
his breathing, when 
deeply anaesthetized, 
will be unrestricted. 
The operator makes 
his incision in the mid¬ 
line through the skin 
and fascia, of such a 
length as will enable 
him to work upon the 
spinous processes of 
the diseased vertebra? 
and upon those of one 
or two vertebra? above 
and below them. Previ¬ 
ous to the operation, of course, the exact extent of the 
disease has been determined by the Rontgen rays. The 
skin is then shut off with towels. Hibbs towel clamps 
make this easy and rapid. From now on three rules will 
be found helpful: 


. V 


Fig. 79.—Incisions for the Hibbs and Albee oper¬ 
ations. The solid line is the Hibbs incision, the 
dotted line the Albee. 


0 Ely, Leoxard W.: “Ankylosing operations on the spine, etc.” Jour. 
A. M. A., 1917, lxviii, 183. 






TUBERCULOSIS OF THE SPINE 


255 


1. Take plenty of time. Do not try to hurry, but do 
the dissection carefully. 

2. In the first part of the work keep exactly in the mid- 
line, and so avoid hemorrhage. If this and the next rule 
he observed, hemostasis will not be necessary. 

3. In all skeletonizing, keep close to the bone. The 
instant one gets away from it, one cuts blood vessels which 
must be tied. 

The next step is to incise the periosteum over each 
spinous process, and to push it back for a short distance. 
Small pieces of gauze are then tucked tightly under the 
periosteum, checking bleeding and pushing the periosteum 
back still farther. The tips of all the spinous processes 
to be operated upon are to be laid bare before proceeding 
to the next step. 

Insert a small scalpel close to the last spinous process, 
and divide the interspinous ligament between it and the 
spinous process next higher up, exactly in the mid-line. 
Divide in the same manner the interspinous ligament of 
all the spines to be operated upon, and dissect the peri¬ 
osteum from one side of the spinous processes, and from all 
the laminae on one side, packing the wound behind you with 
larger pieces of gauze as you go. The assistant in spong¬ 
ing aids the dissection by pushing the periosteum off the 
hone as he sponges. The dissection is carried laterally 
as far as the lateral articulations, whose location and plane 
have been ascertained on the skeleton if necessarv, before 
the operation was started. Divide the ligament of each 
lateral articulation, and scrape it out thoroughly with a 
small curette. Repeat these procedures upon the other 
side. Be sure to remove every bit of periosteum from the 
spines and the laminae, and bare the upper and lower 
borders of the lamina? of every vestige of the ligamenta 


256 INFLAMMATION IN BONES AND JOINTS 

subflava, working a small curette even somewhat around 
on their anterior aspect. All this takes a great deal of 



Fig. 80.—Tuberculosis of the spine. Crushing together of the bodies 
of the 3rd and 4th lumbar. Note their wedge shape. The disease in 
the stage of healing. A Hibbs operation was performed eighteen 
months previously. Union was not obtained between the 4th and 
5th lumbar vertebrae, and a second Hibbs operation was done nine 
months later. The child now is apparently well. Note the bony 
bridge in the laminae, and the fairly sharp outline of the two affected 

vertebrae. 

time and some anatomical knowledge, and must be done 
deliberately. The rest is comparatively simple. 

With a small Hibbs gouge or chisel inserted at the base 
of the spinous process, chisel a very thin wedge or sliver 








257 


TUBERCULOSIS OF THE SPINE 

ot bone from the lower border of each lamina with its base 
lateral, leaving the base of the wedge intact, and, still 
attached at its base, turn this wedge or sliver down across 
the interlaminar space upon the next lamina below it. 
Hibbs now is varying this by chiseling a flake from the 
posterior surface of the lamina, and turning it upward on 
the lamina above. 

With a pair of Hibbs bone forceps partially divide each 
spine at its base, leaving only its lower or distal portion 
intact, and break each spine down, so that its tip rests upon 
the raw base of the one below it. 

With kangaroo tendon or ten day catgut, suture the 
periosteum and deep fascia in the form of a tube. This 
is best done in stages as the spines are fractured. Suture 
the skin with catgut, and put the patient to bed upon his 
back. As after any operation on bone, if the wound be 
not sewn up too exactly, seepage of blood through it will 
he facilitated, and the formation of a hematoma will be 
discouraged. The wound is dressed after a week or ten 
days. The patient lies flat on his hack for six weeks. 
Hibbs applies a specially made Taylor brace immediately 
after the operation. Children do well on a Whitman- 
Bradford frame. 

For six months after the operation the patient wears a 
Taylor brace, or a plaster jacket. By the end of this time, 
firm bony fusion of the laminae should have occurred, 
though Hibbs advises splinting for about a year. Labora¬ 
tory specimens and secondary operations show that this 
fusion actually does take place. Secondary operations 
show that persistence of pain, and further progress of the 
disease may be due to unskilful operating. In spite of 
apparently unfavorable conditions for wound healing, 

17 


258 INFLAMMATION IN BONES AND JOINTS 

experience shows that infection of the wound is very rare, 
and usually is of little moment when it does occur. 

The Bradford frame is made of gas pipe, covered with 
canvas, in three pieces, of which the middle one under the 



Fig. 81.—Antero-posterior view of the preceding. Note the old calcified psoas abscess. 

buttocks is removable to facilitate the introduction of the 
bed pan. This frame is slightly wider than the patient’s 
body. It rests on the bed, and the patient is bound to 
it with a swathe. 

Whitman’s modification of Bradford’s frame is pre¬ 
ferred by many, as affording better immobilization. Its 








259 


TUBERCULOSIS OF THE SPINE 

frame also is of gas pipe, usually of a calibre of three- 
eighths to a half inch, with ordinary elbows at the four 
corners. It is provided with a canvas cover, laced up the 
hack, and with straps at the top and bottom, so that it 
can he drawn very tight. A canvas apron with straps 
attached for insertion into buckles sewn to the canvas cover, 
serves to secure the patient to the frame. This frame is 
much narrower than the original frame of Bradford, having 
a width equal to the distance between the patient’s shoulder 
joints, and a length about eight inches greater than his 
height. It is very convenient for carrying the patient 
about, and affords perhaps better immobilization for the 
spine than any other form of apparatus. A piece of rub¬ 
ber sheeting sewn to the canvas cover under the buttocks 
prevents soiling. It can be easily manufactured by a 
plumber and harness maker. 

The Taylor brace has a framework of two steel upright 
bars attached below to a thin, flat, steel pelvic band, about 
an inch and a half or two inches wide. The steel uprights 
run parallel, about an inch and a half to two inches apart, 
according to the patient’s size, flare slightly outward above, 
and extend to a point just below the upper lateral border 
of the trapezius muscles. They are fitted accurately to 
the curves of the spine, rest upon the lateral masses of the 
vertebra?, and are provided with padding on the side toward 
the body. The pelvic band about half encircles the body 
between the femoral trochanters and the crests of the ilia, 
and it also is lightly padded with leather on its inner aspect. 
The frame is held to the body as a splint, above by means 
of shoulder straps attaching to the steel uprights at their 
top and at their middle, below by an abdominal apron 
buckling by straps to the pelvic band and to the uprights. 

Instead of any of these forms of apparatus a plaster 
jacket may be employed, but great care must be exercised 


260 INFLAMMATION IN BONES AND JOINTS 

to prevent excoriations Qver the fresh wound. A plastei 
bed does not entail so much danger of these. This should 
be made a few days before the operation. With the pa¬ 
tient lying on his face plaster bandages are passed back 
and forth over his trunk, and if necessary over the back of 
his head, and are molded snugly upon him like a shell. 
This shell is put away in a hot, dry place to promote setting, 
and receives the patient after the operation. 

Occasionally persistence of pain after the lapse of time 
sufficient for bony union warns of its failure, perhaps 
between two vertebras only. A second operation will cor¬ 
rect this, but this occurrence becomes less frequent as 
skill increases. 

The Albee Operation. —Prepare the back and the 
right shin for operation. Having ascertained as accu¬ 
rately as possible the extent of the disease, make a curved 
incision long enough to permit operating upon the spines 
of the affected vertebrae and of those of the healthy verte¬ 
bras above and below them—at least of one above and one 
below. The incision starts at about the line of the spines, 
curves laterally for about an inch or more, runs parallel 
to the vertebral column, and curves back again to the line 
of the spines. Dissect the flap back and reflect it. With 
a very broad, very sharp Albee osteotome, chisel deeply 
into the spines, slightly to one side of their middle, and pry 
the smaller piece laterally with the osteotome. The osteo¬ 
tome divides not only the spines but also the interspinous 
ligaments, and leaves a deep wound with the raw fractured 
surfaces of the spines at intervals on its walls. Measure 
with a probe the length of this wound, and bend the probe 
at a point to register the required length of the graft. 
Cover the wound with a towel. 



TUBERCULOSIS OF THE SPINE 


261 


With the right leg flexed at the 
knee, make a slightly curved inci¬ 
sion about an inch longer than the 
length of the proposed graft, over 
the antero-medial cortex of the 
tibia, and reflect the flap. Reflect 
the flap from the crest of the tibia 
rather than towards it. In other 
words make the incision convex 
towards the crest. Make two 
straight parallel incisions, about 
five millimetres apart, through the 
periosteum, whose length is that of 
the proposed graft, and connect 
their upper and lower extremities. 
In other words trace out the graft 
in the periosteum. 

With a very narrow osteotome, 
chisel through the tibial cortex 
transversely at the upper and lower 
ends of the graft. With a motor 



10 


saw/" single or twin, saw through 


the tibial cortex in the line of the 
incision of the periosteum, having 
an assistant pour water on the saw 
meanwhile to keep it from getting 
hot. Remove the graft and grasp it 
with two pairs of Kocher forceps. Turn the wound in the 
leg over to an assistant for closure, or cover it with a towel 
for closure when the rest of the work is done. Wedge the 


Fig. 82. —Specimen removed at 
necropsy from a case of hepatic 
cirrhosis. An Albee spine oper¬ 
ation had been done for spinal 
tuberculosis two years previ¬ 
ously, and a cure apparently 
had resulted. The graft is on 
the left. It had solidly united 
to the spinous processes. A 
section was removed at A for 
microscopical study. 


10 In case of need the graft can be removed with mallet and osteotome, 
but the operation is much more difficult, and the pain after the operation 
is wont to be greater. 



I 


262 INFLAMMATION IN BONES AND JOINTS 

graft between the divided spinous processes, and suture it 
firmly in place with sutures of kangaroo tendon, or chromi- 
cised catgut through the interspinous ligaments. Close 
the wound. Put the patient to bed on his back, and keep 
him there for six weeks. The wound may be dressed in 
a week or ten days. Prudence dictates the application of 
a plaster jacket, or a brace for several months thereafter. 

In favorable cases, new bone is laid down upon the 
trabecula? of the graft, and the spinous processes become 
united with a firm bony bridge. Occasionally the graft is 
cast out, and the operation is a failure. 

In order to avoid the wound in the shin, some operators 
have made use of boiled bone from other animals, but the 
consensus of opinion seems to be that these heteroplastic 
grafts are inferior to the so-called autoplastic. The greater 
ease with which boiled bone is absorbed throws the scale 
against success in a certain proportion of cases. 

XOX-OPERATIVE TREATMENT 

This can be carried out in recumbency on a frame, or 
with some form of ambulatory apparatus, such as the 
Taylor brace or a plaster of Paris jacket. Leather jackets, 
moulded on a plaster cast of the trunk, steel and celluloid 
corsets, etc., have their advocates. 

The frame is especially adapted to young children, and 
to meet special indications in older children, such as the 
onset of a paraplegia, or the occurrence of abscess. To 
adults, whose spines have fixed curves, the frame is not so 
well adapted. The Whitman-Bradford frame, when bent 
backward at the seat of deformity, tends to reduce the 
kyphosis. In the past the forcible correction of the de¬ 
formity, under an anaesthetic, has been advocated on the 
ry ould new bone in the gap left 


TUBERCULOSIS OF THE SPINE 


263 


by the separation of the vertebral bodies, but this she seems 
unable to do. The operation is not without danger, and 
has been generally abandoned. 

The plaster of Paris jacket forms an excellent splint 
for routine employment, and should he put on with the 
patient partly suspended. The ordinary jacket is of little 



Fig. 83.—Ordinary plaster jacket. In the spine of the patient on the left the 
disease is rather high up, and the jacket evidently is not controlling the deformity. 

use in disease above the seventh cervical vertebra and it 
must be made as long as possible, consistent with the use 
of the limbs. The line of its upper border runs from just 
below the upper border of the sternum, curves sharply 
downward at about the nipple line, under the axilke, and so 
across the back. The lower border reaches almost to the 
pubes, then curves upward to allow flexion of the thighs. 




264 INFLAMMATION IN BONES AND JOINTS 

For disease of the upper thoracic or of the cervical 
spine the base of a so-called jury mast can be incorporated 
in the plaster jacket, and from this jury mast the head of 
the child may be slung. It is rather an unsightly, and by 
no means a satisfactory appliance, and has been more or 
less superseded by the “grand” Calot jacket, which pro¬ 
vides support for the chin and occiput. This jacket is not 



Fig. 84. Calot head sling. One safety pin has been inserted. 

easy to make, and the surgeon who has never applied one 
will do well to practise on the mannikin. 

The Calot head sling is an improvement over the old 
fashioned kind, and is made of strips of canvas 6 centi¬ 
metres wide. To a circular piece 168 centimetres in cir¬ 
cumference, is sewn a tail piece 104 centimetres long, at 
right angles to it. With the tail piece exactly in the middle 
the circular piece is laid flat upon the table. This gives 
the contrivance a T-shape, with the doubled circular strip 
for the cross piece. If the patient’s occipitofrontal cir- 
cumference be taken, if two centimetres be added to this, 
if one quarter of this distance be measured off on each side 
from the middle of the tail piece along the circular strip, 
and if the circular strip be fastened together with safety 























TUBERCULOSIS OF THE SPINE 265 

pins at these points, a sling results which can be just slipped 
over the patient s head under his chin and occiput. The 
part of the circular strip on the outside of the safety pin 
passes up at the side of the patient’s head, and with its 
fellow on the other side serves as a sling to suspend the 
patient from a cross bar. The tail piece starts from the 
child’s occiput, and passes up to be attached to the middle 
of the transverse bar. It keeps the patient’s head from 
tilting backward, when his heels are pulled clear of the floor. 

The patient wears two shirts of stockinette, the inner 
one provided with short sleeves, and long enough to be 
pinned over the top of the head during the application of 
the jacket, the outer one sleeveless, and reaching to the 
neck. A nose hole is cut in the inner one to allow free 
breathing. The chin, occiput, pelvis, and the kyphosis are 
then well padded, and a large triangular pad of cotton 
wadding, or of cotton batting, about an inch thick, is held 
in place by an assistant, over the sternum and the anterior 
aspect of the ribs. Another assistant holds the patient’s 
arms at an angle of about 45 degrees to his body. Two or 
three plaster bandages are then applied rapidly and 
smoothly to the head, neck and trunk of the patient, leaving 
the breathing hole, of course, free. An assistant slits the 
borders of these bandages with scissors where they tend 
to draw. Then the auxiliary pieces, which an assistant has 
been preparing, are applied, and over these several more 
plaster bandages—enough to give the jacket the required 
strength. 

While the plaster is drying, the surgeon and his assist¬ 
ants give their attention to molding it as accurately as pos¬ 
sible upon the patient, especially about the shoulders and 
pelvis. Through a small triangular opening cut over the 
sternum the large pad of cotton is removed, and the jacket 


266 


INFLAMMATION IN BONES AND JOINTS 



is trimmed off above, below, and at the junction of the 
arms with the body. The line of the jacket above runs 

from just below the mouth, 
curves gently downward to clear 
the ears, and then rather more 
sharply upward again to include 
the occiput. The patient is 
removed from the sling, and is 
laid face downward, with his 
head over the edge of the table. 
A nurse should watch his breath¬ 
ing for a while to see that it is 
not impeded. 

About the end of 48 hours, 
the jacket should be cut out in 
front, as shown in the illustra¬ 
tion. If the surgeon wishes to 
attempt to reduce the deformity, 
he may also cut a window 3x6 
inches over the kyphosis, and, 
having slit the shirt and greased 
the skin, tuck between them 
oblong pieces of cotton wadding, 
somewhat larger than the win¬ 
dow, by means of a spatula. The 
shirt may then be folded back 






Fig. 85.- 


-The “grand” 
jacket. 


Calot 


into place, and the whole thing 
held in place by a plaster band¬ 
age. This procedure tends to drive the kyphosis forward, 
and may be repeated at intervals of two months. A jacket 
should last for about six months. 


The auxiliary pieces mentioned above consist of three 
or four layers of crinoline impregnated with fresh plaster 




TUBERCULOSIS OF THE SPINE 


267 


cream. They are four in number, two aprons, a chin piece, 
and a piece for the occiput. The aprons are one and a 
half times the length of the trunk, 
and in width are equal to one-half 
its circumference. The anterior one 
is applied from the top of the ster¬ 
num to the pubes, and its redundant 
portion is folded up over the lower 
abdomen. The posterior one is slit 
up for almost half of its length, mak¬ 
ing two tails, and these tails are 
brought over the shoulders, and then 
down in front of the chest, and each 
into its own axilla. As with the 
plaster bandages an assistant stands 
ready to nick the aprons with scis¬ 
sors, to make them lie smoothly. 

The pieces for the chin and occi¬ 
put, about 4x6 inches in diameter, 
are applied to the front and back of 
the neck, and reinforce the jacket in 
these regions. 

Pott’s Paraplegia. —This is 
best treated by recumbency, rein¬ 
forced by a frame or perhaps by a 
Calot jacket. The outcome is usually 
good. The operation of laminectomy 
has been recommended by some sur¬ 
geons. Menard advised costotrans- 

versectomv to remove the broken down material on the 
•/ 

outside of the dura. 11 



Fig. 86.—The “grand” 
jacket, side view. 


Calot 


" Goldman^: “ Ueber die chirurgischie Behandlung der Spondylitis tuber- 
kulosa.” Munch med. Woch., 1909, lvi, 2341. 






268 


INFLAMMATION IN BONES AND JOINTS 


Treatment of Cold Abscess. —The secret of the treat¬ 
ment of a cold abscess is to attack it before it grows too 
large, and before it approaches the surface too closely. 
The postpharyngeal abscess may be aspirated from the 
side of the neck, and if the surgeon wishes, he may inject 
its cavity with an iodoform mixture, or with any sterile 
mixture he fancies. Psoas abscesses should be attacked 
before they pass under Poupart’s ligament into the thigh. 
A large aspirating needle is thrust inwards and upwards 
at a point one centimetre distal and two centimetres medial 
to the anterior superior spine. The dressing should be so 
bandaged on as to exert continuous pressure thereafter, 
and the aspiration should be repeated as often as the abscess 
fills. One’s efforts in this line will he more successful if 
the patient he put to bed. Otherwise the force of gravity 
must be combated. 


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TUBERCULOSIS OF THE SPINE 

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Allison, Nathaniel: “ Description of apparatus for the application of plaster- 
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269 


TUBERCULOSIS OF THE SPINE 

Brackett, E. G., and Crandon, L. R. C.: “Observations on the comparative 
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Ely, Leonard W.: “Tuberculosis of the spine.” Internat. Clin., 1919, i, 72. 

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270 INFLAMMATION IN BONES AND JOINTS 

Fickler, Alfred: “ Studien zur Pathologie und pathologischen Anatomie der 
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Finck, J.: “Das allmahliche Redressement des Pottschen Buckels im Liegen.” 
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Londe, Paul: “Double syndrome de Brown-Sequard dans le mal de Pott.” 
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Lortat-Jacob : “Syndrome radiculaire du membre superieur d’origine 
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Marinesco, G.: “ Changements morphologiques des cellules des ganglions 
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driisentuberkulose. . Deut. Ztschr. f. Chir., 1908, xciv, 419. 

Menard, V.: “Causes de la Paraplegie dans le mal de Pott.” Rev. d’ Orth.” 
1894, v, 47. 

Menard: “Considerations anatomiques sur le redressement des gibbosities 
pottiques.” Gaz. Med. de Paris, 1897, 10. ser., 231. 

Morestin, H.: “ Traumatisme du rachis chez un pottique.” Soc. Anat. de 
Paris, Bull., 1902, lxxvii, 577. 

Mosny: “ Meningo-radiculite consecutive a une osteite tuberculeuse. . .” Soc. 

Med. Hop. de Paris. Bull., 1906, xxvi, 1097. 

Mueller: “Studien zur Pathologie und pathologischen Anatomie der Rucken¬ 
markscompression bei Wirbelcaries.” Munch, med. Wchnschr., 1900, xlvii, 
1084. 

Nasse: “ Arbeiten ueber das gewaltsame Redressement der Pottschen 
Kvphose.” Berl. klin. Wchnschr., 1898, xxxv, 13. 


TUBERCULOSIS OF THE SPINE 271 

Osten-Sacken, E. V. D.: “ Ueber Deformierungen des Unterkiefers durch 
Stutzapparate bei Spondylitis.” Ztschr. f. Orth. Chir., 1909, xxiii, 353. 
Packard, F. A.: “Multiple tuberculous tumors. . ” Path. Soc. Phila., Trans 
1895-1897, xviii, 360. 

Steele, A. J. : “Was Percival Pott really entitled to the honor of having 

a certain spinal disease called by his name.” Am. Jour. Orth. Sura., 1906, 
iv, 170. J 

Tillmanns, H.: “Ueber die Entstehung und Behandlung der spondylitischen 
Lahmungen.” Arch. f. klin. Chir., 1903, lxix, 134. 

Wieting, J. : “Ein Fall von ischamischer Riickenmarksaffektion bei tuber- 
kuloser Spondylitis.” Deut. Ztschr. f. Chir., 1903, lxx, 112. 


CHAPTER II 
TUBERCULOSIS OF THE HIP 

While presumably the disease may occasionally start 
in the synovial membrane, the original focus in the great 
majority of cases is probably in the hone. It may be 
in the acetabulum, or more often in the head or neck of 
the femur. If the head and neck of many femora be sawn 
into thin slices, a small area will usually be found in the 
distal and medial portion of the head, near the joint surface, 
in which the bone trabeculae are very scant, and in which 
there is little else but marrow . 1 This seems to be the 
favorite starting place of the disease. 

In rare instances the marrow of the great trochanter 
may be attacked, and the hip joint itself may never be 
invaded at all. As a rule the disease does not travel widely 
in the os innominatum unless secondary infection take 
place, but remains limited to the region of the acetabulum. 
The tuberculous granulations may make their way through 
this, perforate it so to speak, and give rise to an intrapelvic 
abscess. The customary place of exit of a cold abscess 
from the joint is at its distal and medial aspect, where the 
capsule is weak. 

As a result of the pressure of the head of the adducted 
femur on its proximal rim, more or less softened by disease, 
the proximal portion of the acetabulum undergoes partial 
absorption, and the head of the femur becomes subluxated 
proximally, though practically never does actual luxation 
take place. The acetabulum becomes elongated, shaped 

1 Ely, Leonard W.: “A study of 100 dry bones sawn in the laboratory: 
Bone and joint studies, I.” Published by Leland Stanford University, 1916. 

272 



TUBERCULOSIS OF THE HIP 


273 


somewhat like an oyster shell. This is the so-called “wan¬ 
dering acetabulum” of hip joint disease. 

SYMPTOMATOLOGY 

The pain in hip joint disease may be referred to the 
joint itself, or, especially in children, to the medial aspect 
of the knee. In the early stages of the disease, it may he 
worse in the morning, when the patient begins to go about, 
growing better on exercise, but generally it is made worse 
by motion of the joint, as is usual in tuberculous joint 
disease. It is more or less constant, though it may come 
on in spasms at night, and may cause the notorious night 
cries, described in the preceding section. It may cease 
entirely if the joint be immobilized. 

To the pain is also added a feeling of stiffness, and in 
adults the stiffness may be more prominent than the actual 
])ain, and, like it, may be quite marked in the morning, 
wearing off as the limb is used, that is, in the early stages 
of the trouble. The stiffness and the pain cause a limp. 
Muscular spasm is a constant physical sign. The patient 
often complains that one of his legs is shorter than the 
other, usually the affected one. 

When the patient is stripped, and is laid supine upon 
a firm examining table, a change of attitude may be noted, 
sometimes, in the early stages or after the rupture of an 
intraarticular abscess, an attitude of slight abduction and 
external rotation. The characteristic attitude of hip joint 
disease however is one of flexion, adduction and internal 
rotation. The recognition of the attitude of the limb, and 
its interpretation is sometimes difficult to the uninitiated, 
and a few words upon the symptom-complex may he 
in order. 

When the normal child lies supine, his lumbar spine, 


18 


274 


INFLAMMATION IN BONES AND JOINTS 


his hips, and his lower extremities rest upon the table, and 
if his heels are together, his extremities will roll somewhat 
outward, and his feet will be seen slightly to diverge. In 
an adult the lumbar spine is close to the table if it does 
not touch it. This is the normal posture of extension, and 
of slight external rotation, indifferent as to abduction or 
adduction. Any deviation from normal as to rotation can 
be distinguished easily by comparison with the well side. 

If fixed flexion be present, the popliteal space leaves 
the table, and the thigh is seen to be at an angle with the 
trunk; but it must be remembered that the normal lumbar 
spine is flexible, and, if it arches upward, the knee can be 
crowded down upon the table. This will disguise the 
presence of any ordinary degree of flexion in the hip. 
Hence in determining the presence of fixed flexion one 
must be sure that the lumbar spine is flat upon the table. 
It may be held there by flexion of the sound hip. If fixed 
flexion be actually present upon the affected side, the 
knee on that side cannot then be brought down upon 
the table. 

The attitudes of fixed abduction and fixed adduction, 
are not so easily understood, but a little study clears them 
up. Normally in standing or lying, the thighs are neither 
in abduction nor in adduction, but are parallel (Fig. 88 
1, c, d). Now if we suppose that the left thigh is adducted 
(Fig. 88: 2,d), and that the pelvis (b), and the spine (a), 
are fixed and immovable, then the left thigh (d) will be 
crossed over the right thigh, and progression would be 
extremely difficult; but the lumbar spine is flexible, and 
the patient, in order to bring the thighs into line, tilts the 
pelvis up on the affected side (Fig. 87; 31). At the same 
time, it is seen that this manoeuvre throws the sound side 
into abduction, and draws up the affected extremity, so 


TUBERCULOSIS OF THE HIP 


275 


that it looks short —apparent shortening —while measure¬ 
ment with the tape shows that the two extremities are of 
the same length. 


An analogous state of affairs is present when the limb is 
in abduction (Fig. 88; 4 and 5). Adduction makes appar¬ 
ent shortening, abduction makes api^arent lengthening. 




...D 





Fig. 87.—Diagrams showing the effect of fixed adduction and of fixed abduction upon the 

attitude of the lower extremity. 



The change in the attitude of the limb is responsible 
for various physical signs that are often described; e.g., 
if the thigh is in flexion, the gluteal fold will be shorter and 
shallower, and the fold of the groin deeper than on the 
sound side. If the limb is in adduction the fold of the 
groin is deepened, if in abduction it is made shallower. 

The trochanter is at Nelaton’s line, or in old cases with 
wandering acetabulum slightly above it. 

Limitation of motion will usually be present in all 
directions, especially of abduction, and it varies from a 
















276 INFLAMMATION IN BONES AND JOINTS 

slight restriction at the extremes to a practically complete 
abolition of motion. Attempts at passive motion cause 
pain and muscular spasm. 

To elicit the limitation of motion one puts the joint 
through its passive range in every direction, comparing 
each motion with that on the sound side. To ask the 
patient to perform the motions actively is to introduce an 
element of confusion, and subserves no useful purpose. 
It is well to adopt a regular routine, and to follow it 
methodically. With the knee of the affected limb held 
to the table, one flexes the sound hip, with the knee flexed, 
and notes its range. One repeats the manoeuvre with the 
affected hip, and compares the result. Then with the hip 
and knee in right angle flexion one tests the range of 
abduction and of adduction, first in the sound hip, and 
then in the affected one. In the same attitude, and in the 
same way one tests the range of internal and of external 
rotation. Finally, one turns the patient on his face, and 
tests the range of extension in each hip, holding the other 
one flat on the table. 

Sensitiveness and slight swelling can sometimes be 
detected over the head of the bone, and occasionally, thick¬ 
ening about the trochanter. The practice of striking the 
soles of the feet in an attempt to elicit pain is unnecessary, 
and, as it inflicts trauma, is unwise. 

Atrophy of the thigh and of the calf often can be dis¬ 
cerned by the naked eye, but should be accurately deter¬ 
mined with the aid of a tape, measuring at corresponding 
levels on the two sides, that is, at a certain distance from the 
patella. Generally speaking, the atrophy of a tuberculous 
arthritis is greater than that of other forms of arthritis of 
an equal severity. 


TUBERCULOSIS OF THE HIP 


277 

It is customary to determine the actual shortening or 
lengthening by measuring from the anterior superior spine 
to the tip of the medial malleolus, and, while this measure¬ 
ment is not accurate, it is sufficient for all practical pur¬ 
poses. In the early stages of the disease a slight increase 
of length can sometimes be detected, probably the result 
of stimulation of growth caused by the inflammatory proc¬ 
ess close to the epiphysial disc. Thereafter growth lags 
behind, and measurement shows an actual shortening. 
This shortening is rarely great, usually about a centimetre 
or two, but it persists through life. It is due to three 
things: 1st. Interference with growth at the epiphyseal 
disc, 2nd. Destruction of much or little of the head of the 
femur, 3rd. Subluxation of the head proximallv in the 
wandering acetabulum. Parenthetically it may be re¬ 
marked that the left lower extremity is usually longer 
than the right. 

Measurement from the umbilicus to the medial malleoli 
shows the apparent shortening or the apparent lengthening. 
As far as the patient himself is concerned, the apparent 
lengthening or shortening is the practical lengthening or 
shortening; for if the extremity be drawn up, it is function¬ 
ally short as well as apparently so, and the patient will 
always complain that his leg is short. 

DIFFERENTIAL DIAGNOSIS 

What already has been said in the section on the general 
differential diagnosis, applies to the hip. Several lesions 
however deserve special mention. 

In congenital dislocation the limp will have been 
present from infancy, that is, from the time the child began 
to walk. The joint will not be painful, muscular spasm and 
signs of inflammation will be absent, abduction alone will 


278 


INFLAMMATION IN BONES AND JOINTS 


be limited, the shortening will amount to an inch or more, 
and finally, the head of the bone will be found both by 
palpation and by the Rontgen rays, to be out of its socket. 

Legg^s disease, the so-called Perthe’s disease, “arthritis 
deformans juvenilis ” gives a clinical picture very like that 
of tuberculosis. Only during the last few years have the 
two been differentiated. It is probably the recovery of 
patients with Legg’s disease, that has made certain sur¬ 
geons optimistic in their view of hip joint tuberculosis. In 
Legg's disease, the patient, usually a boy between five and 
ten years of age, complains of a painless limp. The hip 
is usually in slight external rotation, and, when it is flexed, 
goes into slight abduction. Muscular spasm is very slight, 
if present at all. Abduction is greatly limited, other 
motions may he limited or free. The diagnosis is made 
with the aid of the X-rays. In Legg's disease, most of 
the change takes place in the epiphysis itself, which becomes 
flattened, segmented, and often displaced laterally. Areas 
of rarefaction may or may not appear in the neck, which 
becomes shortened, thickened, and often bent at a more 
acute angle with the shaft—coxa vara. 

Coxa vara (bending of the femoral neck) is a disease, 
or rather a deformity of adolescence, causing limp, limita¬ 
tion of motion, stiffness and some pain. Its cause in the 
great majority of cases is probably an old unrecognized 
Legg’s disease, or an old healed fracture of the femoral 
neck. In localities where joint conditions receive proper 
attention this condition is not seen as often as formerly. 
The limb is in an attitude of adduction, extension and 
outward rotation, while abduction, flexion and internal 
rotation are limited. Actual shortening of one to two 
centimetres is present, the trochanter is prominent, and the 
X-rays show the head of the femoral head in the socket, 



TUBERCULOSIS OF THE HIP 


279 


and the neck at a more acute angle with the shaft 
than normal. 

Psoas contraction is sometimes mistaken for hip joint 
disease, but with psoas contraction the hip is not adducted 
nor rotated inward, and when the psoas-iliacus muscle is 
relaxed by flexion of the thigh, all hip motions except 
possibly internal rotation are unrestricted. Again, an 
examination of the spine will often reveal the evidences 
of Pott’s disease with psoas contraction. 

PROGNOSIS 

This is quoad vitam, good. Secondary infection with 
extensive suppuration in the os innominatum puts the issue 
in doubt. As to function authorities differ. Some sur¬ 
geons believe in their ability to cure the disease by conserva¬ 
tive treatment with excellent function, others, of which the 
author is one, think that a stiff hip or a loose one with an 
amputated femoral head is the best that can be attained. 1 ' 

TREATMENT 

Here again authorities differ. Some advocate radical 
measures in patients of all ages, others invariably carry 
out conservative treatment. Practically all agree that half 
way operative measures, such as scraping, draining and 
packing are worse than useless. The trend of modern 
opinion is toward conservative treatment in children and 
radical treatment in adults. The principles on which each 
is carried out have been set forth in the section on joint 
tuberculosis in general. The special measures for carry- 

2 On page 133 of the author’s book on joint tuberculosis, appears a 
Rontgen picture of a supposed case of hip joint tuberculosis cured with 
perfect function. In the light of modern knowledge this is evidently a 
case of Legg’s disease. 





280 INFLAMMATION IN BONES AND JOINTS 

ing out these principles in disease of the hip will be 
detailed here. 

Conservative Treatment.— In an early case, without 
deformity, splinting may be resorted to forthwith, other¬ 
wise the first indication is to remove the deformity. This 
may be done in one of several ways. 

1. Rest in bed with traction. This is done with an 
ordinary Buck’s extension outfit. In order that traction 
may be made in the line of deformity, the affected limb is 
flexed until the lumbar spine lies flat upon the bed, and 
then is supported by an inclined plane. As the spasm gives 
way, and as the fixed flexion lessens, the inclined plane is 
lowered until the limb rests upon the bed. The reduction 
of the deformity is made easier if a hip splint is first applied. 
Traction may then bemade upon the lower end of the splint. 

2. Slow correction with plaster of Paris spicas. With 
assistants holding the limb in the best possible position, a 
well padded plaster spica is applied from the nipple line 
to the toes. This plaster remains on for several weeks. 
When it is removed, the deformity will be found capable 
of partial reduction. Another spica is then applied in the 
improved position, and others follow it until the deformity 

•7 

has been entirely corrected. This is the method of Lorenz, 
somewhat tedious, but safe. 

3. Immediate reduction of the deformity under ether , 
followed by the application of a plaster spica, or of a hip 
splint, with succeeding rest in bed. This method has its 
disadvantages, and, on account of the unavoidable trauma 
to the inflamed joint, is not without danger, but if the 
manipulation be carried out with strong traction, and very 
gently and carefully, the results are usually good. It is 
especially indicated where the deformity is caused by mus- 
cular spasm, rather than by adhesions in the joint. 


TUBERCULOSIS OF THE HIP 


281 



The deformity we are compelled to fight throughout 
the course of a hip joint tuberculosis, is one of flexion and 
adduction. Therefore we get the hip into an attitude of 
slight abduction (about 20 de¬ 
grees) and full extension, and 
endeavor to keep it there. 

After the correction of the 
deformity, the conservative treat¬ 
ment consists in rest for the joint 
until nature has cured the dis¬ 
ease, meeting meanwhile any 
complications that may arise, 
and, according to the individual 
preference of the surgeon for 
immobilization or for traction, he 
will rely mainly upon 1, plaster 
of Paris, or 2, braces. 

1. The short plaster of Paris 
spica in the treatment of hip dis¬ 
ease was introduced by Lorenz 
about 1891, and has attained 
rather a wide vogue. It is now 
the routine treatment in many 
hospitals and clinics. It enables 
the patient to use the limb in 
walking, and so avoids the 
extreme atrophy that accom¬ 
panies the treatment by braces. It is also more 
comfortable and less troublesome than the brace. With 
the hip in plaster the patient can go about and even 
play, and his general condition will usually be better than 
if he be hampered by a heavy brace. On the other hand, the 
protection afforded to the joint by a well fitting brace, is 


Fio. 88.—The short plaster of Paris 
spica in the treatment of hip-joint 
tuberculosis. 




282 INFLAMMATION IN BONES AND JOINTS 

thought by some to be more thorough, and better functional 
results have been claimed for it. The claim has also been 
made that with its use abscesses are rarer. 

The application of a spiea is made easy by the presence 
of a special fracture table, but portable and stationary 
pelvic rests are almost as serviceable, and can be used with 
any common strong table. The head and shoulders can 
rest u])on an ordinary box. Two assistants are advisable, 
one to hold the head and shoulders on the shoulder rest, the 
other to stand between the legs and hold them in position. 
The former is not necessary, the latter is; he gives his atten¬ 
tion to keeping the affected hip in extension and abduction. 

The stockinette shirting reaches from the nipples to the 
malleoli, like a long pair of drawers with one leg cut off. 
The bony prominences of the pelvis and of the knee 
should be well padded with sheet wadding, silence cloth, or 
some similar material. No padding is necessary or advis¬ 
able for the thigh muscles. A snug bandage holds the 
padding in place. 

The plaster bandages are then applied, reversed repeat¬ 
edly and piled up over the pubes, so that the plaster there 
will be about an inch thick, while at the knee its thickness 
will not amount to more than about one-eighth of an inch. 
While it is being applied it is thoroughly rubbed and 
molded, especially about the pelvis, and then it is trimmed 
with a sharp knife in the following manner: Above, at 
the side, the line starts about two inches above the iliac crest, 
and sweeps down across the belly with concavity upward, 
so as to lay bare the umbilicus, and then rises to the former 
level on the other side, and so straight across the back to 
the starting point. 

Below at the knee the plaster holds the condyles and the 
patella, and is cut with a concavity behind so as to permit 


TUBERCULOSIS OF THE HIP 


283 


flexion of the knee. Finally a third cut starts from below 
the level of the trochanter on the well side, and, arch¬ 
ing across just at the pubes, passes two or three 
inches below the perineum, and then under, upward and 
across, clearing the anus by two or three inches, to the 
starting point. 

After the superfluous padding has been trimmed away 
with bandage scissors or Lorenz shears, the shirting is 
turned up over the plaster and sewn to¬ 
gether, so as to make a covering as well 
as a lining. “Scratch” bandages under the 
shirting will keep the skin in condition. 

If one desire to relieve the hip of weight 
bearing one includes the leg in the plaster, 
and in the lower part includes the bars 
of some such appliance as a Lorenz stir¬ 
rup. In this case the sole of the shoe on 
the sound side should be raised two or three 
inches by cork or wood to compensate for 
the extra length. The same effect can be 
obtained without the stirrup if the high 
shoe be worn on the sound side and the 
patient use crutches. 

The Thomas hip splint, not to be con¬ 
fused with the more celebrated knee 
splint, is designed to afford fixation and not traction, 
and is therefore similar in its action to the plaster 
spica, though probably not so efficient, and more 
troublesome. It is not designed to permit weight 
bearing, and with it the patient wears a high shoe on the 
sound side, and goes on crutches. It consists essentially 
of a flat, longitudinal bar, reaching from the level of the 
nipple to the middle of the calf. This bar is carefully 
fitted, and passes straight down posteriorly, behind the 











































284 INFLAMMATION IN BONES AND JOINTS 

tuberosity of the ischium. Three attached horizontal 
bands above, below, and about one-third from the bottom, 
partially encircle the thorax, the upper part of the thigh 
and the calf. This apparatus is bandaged on the patient, 
and a sling over the shoulders from the top cross piece, 
keeps it from sliding down. It is quite popular in Eng¬ 
land, but is rarely used in America. 

The traction brace consists essentially of a leather- 
covered steel pelvic band which partly encircles the pelvis 
just above the trochanters, and of a steel stem running 
downward from the lateral aspect of the pelvic band, 
and at a slight angle with it corresponding to the inclination 
of the pelvis, to a point two and a half to three inches below 
the sole of the foot, where it is turned inward to form a 
foot plate. At the level of the knee the upright is provided 
with a band which encircles the knee, and steadies it. 

The traction is exerted by means of long strips of mole¬ 
skin adhesive plaster on the medial and lateral aspects of 
the thigh and leg, provided at their lower extremities with 
buckles. To the foot piece of the brace are attached straps 
which buckle on these. Counter-extension is furnished by 
perineal bands, which buckle in front and behind to the 
pelvic band, in front directly over the origin of the adduc¬ 
tor muscles;-behind, somewhat further lateral, so that the 
hands will pass over the tuberculosities of the ischia. The 
foot piece is usually shod with rubber or leather to prevent 
slipping. The perineal bands may be made of stout web¬ 
bing covered with two or three layers of Canton flannel to 
prevent chafing. 

Many modifications of this brace have been devised. 
Sometimes the pelvic band is jointed to the upright, some¬ 
times it is bolted fast. The upright may be provided with 
a rack and pinion for extension, perineal bands may be 


TUBERCULOSIS OF THE HIP 


285 



replaced by a padded ring (Thomas ring) about the prox¬ 
imal end of the thigh, or there may be but one perineal 
band instead of two. Sometimes the pelvic band is rudi¬ 
mentary, sometimes the upright is provided with a lateral 
traction strap designed to pull 
the femoral head away from 
the socket. 

The brace sometimes known 
as the Children’s Hospital brace, 
of Boston* has no pelvic band nor 
perineal straps, but instead an 
incomplete ring about the top of 
the posterior portion of the thigh, 
continued by a sort of U-shaped 
piece over the pubes on to the peri¬ 
neum of the sound side. 

With any form of traction 
brace the sole of the shoe on the 
well side should be raised two to 
three inches to compensate for the 
length of the brace. 

It is seen that none of these 
braces immobilizes the hip joint, 

and the whole theory of the trac- Fig. 90.—Ordinary old fashioned 
tion brace rested on the idea 

of “motion without friction. Its advocates belie\ ed 
that immobilization promoted ankylosis, and that a 


certain degree of motion was beneficial. I his theoiy 
was later somewhat modified, and motion was regarded, 
while not actually beneficial, at least, as harmless. 

Attempts have been made to devise apparatus which 
should combine traction with immobilization, but the appa¬ 


ratus was so cumbrous that it never attained wide use. 














286 


INFLAMMATION IN BONES AND JOINTS 


If, in spite of our efforts, cure finally takes place with 
the hip in a faulty attitude of flexion and adduction, no 
attempt should be made to correct the deformity by force. 
To tear loose the dense fibrous adhesions which hold the 
bones fast is, in the hip as in other joints, to run the risk 
of lighting up the disease afresh. In this fibrous tissue 
are locked up collections of tuberculous material. To 
tear it apart is to break down the barriers which nature 
has erected. For the same reason any mobilizing operation 
whatever is to be avoided. It is true that successful arthro- 
plastic operations have been done on old, supposedly 
tuberculous joints, but it is also true that they have lighted 
up disease in old tuberculous joints, long quiescent. 

Probably the safest and most satisfactory operation 
in these old flexed, adducted hips is an osteotomy. It may 
be done in one of several ways. Perhaps the best two 
methods are those by cuneiform osteotomy at the lesser tro¬ 
chanter, and by linear osteotomy through the femoral neck. 
If a linear osteotomy be done at the level of the lesser 
trochanter, the proximal end of the distal fragment is likely 
to be levered medially when the deformity is corrected. 

Cuneiform Osteotomy. —The operator, having gotten 
his bearings on the location of the lesser trochanter, by 
measuring on the X-ray plate, makes his longitudinal inci¬ 
sion, about 10 centimetres long, over the postero-lateral 
aspect of the femur, through the periosteum, down to the 
bone. His assistant retracts the periosteum, and with an 
osteotome he removes a wedge of bone with its apex at the 
lesser trochanter, and its rather broad base at the postero¬ 
lateral femoral cortex. The apex does not include the me¬ 
dial cortex. It runs down just to it. The distal plane of 
the wedge is exactly transverse to the shaft, the proximal 
oblique. The surgeon, by forced abduction and extension. 


TUBERCULOSIS OF THE HIP 


287 


fractures the medial cortex, corrects the deformity, closes 
the wound, dresses it, and applies a plaster spica from nip¬ 
ples to toes. At the end of about five weeks, the leg part 
ol the spica, and about four or five inches of the top, may 
be removed, and the patient may begin to walk shortly 
thereafter. If the limb be put up in an attitude of mod¬ 
erate over abduction, the actual shortening will be compen¬ 
sated, and the patient will walk with a barely perceptible 
limp. The result is a satisfactory one; the disadvantage 
is the unsightly anterior protrusion of the proximal frag¬ 
ment. In a woman it is well to err on the side of 
overabduction. 

A good incision for osteotomy of the neck is a straight 
one 15 centimetres long, from the anterior superior spine 
distally between the tensor fascke femoris and the sartorius. 
It is carried down to the neck, the tissues are retracted, 
and the neck is divided with mallet and osteotome. Dres¬ 
sings and spica are applied as in the preceding operation. 
Some authorities discountenance this operation on account 
of the risk of lighting up the disease, 3 but if bony union 
ensue, the danger is probably very slight. A fracture table 
makes this operation and the preceding quite simple. 

OPERATIVE TREATMENT 

Unless the surgeon cling to the old and discredited idea 
of scraping out and draining a tuberculous joint, or unless 
he throw up the sponge and amputate, he will approach the 
problem with one of three ideas in his mind. He will 
endeavor (a) to remove all the tuberculous tissue, (b) to 
ankvlose, or (c) to resect and (1) dislocate, or (2) shove 
the trochanter into the acetabulum. 

3 Vincent, Eugene: “ Osteotomie et ostectomie pour ankylosis vicieuses 
de la hanche.” Revue de Chir., 1902, ii, 465. 



288 


INFLAMMATION IN BONES AND JOINTS 


(a.) The practical impossibility of removing all dis¬ 
eased tissue from a tuberculous joint already has been 
explained, and yet operations done with this purpose often 
are successful, not because the theory on which they are 
done is correct, but because they accomplish a result which 
was not in the operator’s mind. They vary from a simple 
“tunneling” operation through the lateral cortex into the 
neck, 4,5,6 to a wide resection of the head, neck, greater 
trochanter and acetabulum. Every effort is made to fol¬ 
low the disease with chisel, gouge, knife and scissors, and 
then usually the stump of the femur is thrust into what 
remains of the acetabulum, the wound is closed and dressed, 
and a plaster spica is applied with the limb in abduction. 

( b .) The hip is not an easy joint to ankylose, and, 
before attempting to ankylose it, the surgeon should decide 
whether the patient’s mode of life will be best subserved 
by a perfectly stiff hip, or a loose but fairly stable one. 
If the former, the Albee operation perhaps is the best, if 
the latter, then the hip should be resected. Most operators 
prefer the resection. 

The Albee Operation . 4 5 6 7 —The ordinary anterior inci¬ 
sion, 15 centimetres long, distal from the anterior superior 
spine between the sartorius and the tensor fascial latas, 
is carried down to the capsule, and the capsule is 
opened. With mallet and osteotome, a slice is removed 
from the proximal portion of the acetabulum, and a cor¬ 
responding slice from the proximal portion of the femoral 

4 Macnamara, Charles: “ Diseases of the bones.” London, J. and A. Chur¬ 
chill 1881. 

5 Huntington, T.: “The early operative treatment of osteomyelitis in 
the femoral head and neck.” Surg., Gyn. Obst., 1906, ii, 409. 

6 Sherman, H.: “Report of focal operations in hip joint tuberculosis.” 
Cal. S. J. Med., 1907, v, 62. 

7 Albee, T. H.: Surg., Gyn. and Obst., 1910 x, 256. 





TUBERCULOSIS OF THE HIP 


289 


head. This permits a slight subluxation proximally, of 
the head of the femur. As much as possible of the carti¬ 
lage is removed from the femoral head together with a 
little of the bone underlying it. An assistant rotates the 
femur in and out, to facilitate this. The wound is closed 
with superficial and deep sutures, and dressed. A long 
plaster spica is applied, with the hip in slight flexion 
and abduction. 

Resection. —A simple resection of the femoral head 
in an uninfected case of hip tuberculosis can usually be 
relied on for a cure, whether the operator lets the great 
trochanter dislocate on the dorsum of the ilium, or shoves 
it into the acetabulum. The latter operation is not so apt 
to be followed by extreme and troublesome adduction, as 
the former. We do not know the exact reason why these 
simple operations, without any pretense of removing all 
the tuberculous tissue, are a success, and we shall not know 
until we have had the chance to examine specimens from 
cured cases in the laboratory. Probably the same change 
of the lymphoid marrow to fatty as follows an ankylosis, 
takes place here and the bone becomes dense. Dense bone 
is a poor location for tuberculosis. The disease seems to 
require some space to thrive. Any one of a number of 
incisions may be employed for this operation. 8 The 
wound should always be closed without drainage, and the 
hip should be put up in a long spica in rather marked abduc¬ 
tion. The plaster may be trimmed for 5 or 6 inches above, 
and at the knee, in about a month, and the patient may walk 
shortly thereafter. 

The anterior incision has already been described. It 
does not afford a wide view of the joint, and, if much 

8 Bracket, E. G.: “A study of the different approaches to the hip joint, 
with special reference to the operations for curved osteotomy and for 
arthrodesis.” Boston Med. and Surg., Jour., 1912, clxvi, 235. 


19 



290 


INFLAMMATION IN BONES AND JOINTS 


obstruction to removing the head of the bone exists, it is 
not very satisfactory. The operator who employs it should 
take care to keep lateral to the sartorius muscle. If he 
carry his dissection medial to it he is likely to have trouble 
with branches of the femoral nerve. It is an excellent inci¬ 
sion for a simple case. 

Sprengei/s Incision . 0 —This was brought out many 

years ago, and has recently been revived 
under the name of Smith-Peterson. It 
is very simple, very satisfactory for all 
ordinary cases, and has not attained the 
popularity it deserves. It has two arms. 
The longitudinal one starts from the 
anterior superior spine of the ilium, and 
runs distal about 15 centimetres just 
lateral to the tensor fasciae lata?. The 
transverse arm runs from the anterior 
superior spine backward along the outer 
lip of the crest of the ilium for about 
half its length, and is carried down right 
through the periosteum to the bone. 
Keeping close to the bone, the operator 
then pushes with a blunt chisel the fibres 
of the glutei, medius and minimus, away 
from their attachment to the dorsum of 
the ilium, and reflects backward the 
whole flap of skin, fascia, fat and muscle, until he 
reaches the antero-proximal border of the acetabulum. 
Meantime he has been carrying the longitudinal arm of the 
incision by intermuscular dissection down to the capsule of 
the joint. He opens the capsule and an assistant by exter- 

9 Sprengee: “ Zur operativen Nachbehandlung alter Huftresectionen.” 
Archiv. f. klin. Clnr., 1898, lvii, 837. 



Fig. 91. —Incisions for hip 
joint resection. A, B, ordi¬ 
nary anterior incision E, A, 
B, Smith-Peterson incision. 
E, A, D, Sprengel incision. 
S, sartorius muscle. T, tensor 
fasciae femoris. The dotted 
lines C, A, shows the crest of 
the ilium. 








TUBERCULOSIS OF THE HIP 


291 


nal rotation turns the head out of its socket. It is best to 
remove it at the very base of the neck. If there be any diffi¬ 
culty in disarticulating, the removal of a little bone from 
the antero-superior border of the acetabulum overcomes it. 
My experience with this incision has been veiy satisfactory, 
and I recommend it for routine work. 

After removal of the head, the trochanter may be per¬ 
mitted to dislocate, or it may be shoved into the acetabulum. 
The wound is closed and dressed, and the whole limb is 
put up in a long plaster spica, in a position of ex¬ 
treme abduction. 

Kocher^s Incision. 10 — Place the patient on his sound 
side in the latero-ventral position. Slightly flex the hip. 
Let an assistant grasp the leg so as to change the position 
of the thigh according to directions. 

Beginning at the posterior margin of the base of the 
trochanter major, make a cut in the proximal direction 
to the posterior angle of the summit of the trochanter. At 
this point change the direction of the incision, and cut prox- 
imally and backward towards the posterior superior iliac 
spine, i.e.j cut parallel to the fibres of the gluteus maximus 
and expose that muscle. Split the tendon of the gluteus 
maximus in the direction of its fibres, and enlarge the deep 
wound proximally and backward by splitting the muscle 
itself. Betract the edges of the deep wound, exposing the 
gluteus medius at its insertion into the trochanter. 

Botate the hip slightly inward, so as to make prominent 
the posterior part of the summit of the trochanter. Find 
the groove between the gluteus medius and minimus , prox¬ 
imally, and the pyriformis, distally. Beginning at this 
place separate with elevator or knife the insertions of the 
gluteus medius and minimus, along with the corresponding 


10 From Binnie’s Operative Surgery. 




29 2 


INFLAMMATION IN BONES AND JOINTS 


periosteum, from the trochanter, until the anterior inter¬ 
trochanteric line is reached. At this point separate the 
insertion of the iliofemoral ligament. While doing this 
flex the thigh and rotate it out. 

Divide the capsule along the distal edge of the pyri- 
formis tendon. Flex the thigh and rotate it inwards so 

as to gain access to and divide the 
insertion of the pyriformis. With ele¬ 
vator or chisel (removing a thin shell 
of bone if desired) separate the inser¬ 
tions of the obturators and the gemelli. 

Murphy 11 employed a lateral U- 
shaped incision, with the trochanter in 
its centre, reaching from a point ten 
centimetres proximal to one five centi¬ 
metres distal to the tip of the trochan¬ 
ter. The open end of the U is 
proximal and is twelve centimetres 
wide. He reflected proximally the 
U-shaped flap of skin, superficial fas- 
Murphy incisions for resection cia and fascia lata. He then passed a 

of the hip. A, B, Murphy. C, 

e>, Kocher. Gigli saw about the base of the tro¬ 

chanter, and divided the trochanter. (This may be done 
with osteotome.) The trochanter, with its attached muscles, 
he turned proximally, and thus gained access to the capsule. 



REFERENCES 

TUBERCULOSIS OF THE HIP 

Allison, Nathaniel: “Tuberculosis of the hip. An analysis of twenty-five 
selected cases.” Am. Jour. Orth. Surg., 1914-1915, xii. 622. 

Annandale, T.: “On the pathology and operative treatment of hip 
disease.” Eclinb. Med. Jour., 1875-1876, xxi, 410, 487, 591, 694. 


11 Murphy, John B.: Journal of A. M. A., 1905. 





TUBERCULOSIS OF THE HIP 293 

Ashurst, J., and Tunis, J. P.: “Tuberculosis of the hip-joint.” Path. Soc., 
Phila., Trans., 1898, xviii, 2. 

Bally, R.: “Coxa vara tuberculosa.” Arch. f. klin. Chir., 1907, lxxxiii, 648. 

Barker, A. E.: “The after-history of 41 cases treated by operation for 
destructive hip-joint disease.” Lancet, 1900, i, 1499. 

Beck, Emil G. : “Treatment of tuberculous hip-joint disease with coexisting 
sinus by means of bismuth paste. . .” Western Surg., Ass. Trans., 1913, 
xxiii, 46. 

Binder. R.: “Die conservative Behandlung der Coxitis u. s. w.” Ztschr. f. 
orthop. Chir., 1899, vii, 276. 

Bloodgood, J. C.: “ Early exploratory operations in tuberculosis of the hip.” 
Johns Hopkins Hosp. Bull., 1900, xi, 11. 

Bowlby, A. A.: “Nine hundred cases of tuberculous disease of the hip.” 
Brit. Med. Jour., 1908, i, 1465. 

Bradford, E. H.: “Use of traction in hip disease.” slm. Jour. Orth. Surg., 
1905-1906, iii, 199. 

Brackett, E. G.: “An experimental study of distraction of the hip-joint.” 

Boston Med. Surg., Jour., 1890, cxxii, 241. 

Bruns, P.: “ Ueber die Ausgange der tuberkulosen Coxitis bei conservativer 
Behandlung.” Arch. f. klin. Chir., 1894, xlviii, 213. 

Chipault, A.: “ Coxalgie tuberculeuse limi'tee au ligament rond.” Soc. Anat. 
de Par., Bull., 1890, Ixv, 276. 

Coudray, P.: “ Coxotuberculose et son traitement.” Rev. de Chir., 1911, xliii, 
420. 

Dittle: “ Experimented Studien uber die Stellung bei Hiiftgelenkenzundung 
(Coxitis).” Ztschr. d. k. k. Gesell. d. Aerzte zu Wien., 1856, xii, 665. 
Ehringhaus, Otto: “ Zur Aetiologie der Knochenatrophie bei tuberkuloser 
Koxitis.” Charite-Ann., 1910, xxxiv, 755. 

Froelicif: “ Des coxitis et coxalgies frustes de l’enfance etc.” Rev. de Chir. 
1917, liii, 307. 

Gauvain, H. J.: “Tuberculous disease of hip-joint.” Lancet, 1918, ii, 666 
Gibney, V. P., Waterman, J. H., and Reynolds, W. G.: “A contribution 

to the study of hip-disease. On the ultimate results of the mechanical 
and operative treatment. . .” Ann. Surg., 1891, xxviii. 435, 454. 

Haberern, J. P.: “Ueber Beckenabscesse bei Coxitis und ihre Behandlung.” 
Centrlbl. f. Chir., 1881, viii. 193. 

Hagen, W.: “Zur Statik des Schenkelhalses.” Beitr. z. klin. Chir., 1908, lvi, 

627. 

Jottkowitz, P.: “Die Schleimbeutelentzundungen an der Hiifte in ihrer 
Stellung zu einen Trauma und hinsichtlich der Differentialdiagnose 
gegeniiber einer Coxitis.” Med. lclin., 1918, xiv, 694. 


294 


INFLAMMATION IN BONES AND JOINTS 


Judson, A. B.: “Historical notes on the question of the value of traction in 
the treatment of hip disease.” N. Y. Med. Jour., 1893, lviii, 649. 

Keppler, W., and Erkes, F.: “ Ueber den Wert der Tuberkulinherdreaktion 
fur die Diagnose unklarer Htiftgelenkserkrankungen.” Arch f. klin. chir., 
1914, cic, 800. 

Kocher, T.: “ Arthrotomia coxae.” Arch. f. klin. Chir., 1888, xxxvii, 797. 

Konig: “ Untersuchungen iiber Coxitis.” Deutsche Ztschr. f. Chir., 1873, iii, 
256. 

Konig: “Die operative Entferung (Resektion) des tuberkulos erkrankten 
Huftgelenks ” Berl. klin. Wchnschr 1909, xlvi, 429. 

Maragliano, D.: “La Remeralizzazione Chirurgica delle Coxiti tubercolari.” 
Riforma Med., 1919, xxxv, 292, 394. 

Stempel, W.: “Das Malum coxae senile als Berufskrankheit und in seinen 
Beziehungen zur socialen Gesetzgebung.” Deutsche. Ztschr. f. Chir., 1901, 
lx, 265. 


CHAPTER III 


TUBERCULOSIS OF THE KNEE 

The primary focus may be in the tibia, the femur, or 
the patella. Perhaps in rare instances, the disease may 
start in the head of the fibula. Most authorities agree that 
primary synovial tuberculosis is fairly frequent, and, while 
this theory is practically impossible of demonstration, I 
believe that it is correct, especially in adults. Sometimes 
the location of the primary focus can be detected with 
reasonable certainty, often it can only be surmised. 

The knee joint may be considered as comprising three 
articulations, two tibio-femoral, and one femoro-patellar, 
and this more or less complex arrangement, coupled with 
the presence of the synovial curtains, or partitions, is often 
responsible, in knee joint tuberculosis, for a peculiar dis¬ 
tribution of the disease which has not received the attention 
it deserves. Thus one finds, for instance, cases with 
marked involvement of the quadriceps pouch, and with the 
tibio-femoral articulation practically intact, as if it had 
been walled off by adhesions in the same way as is the peri¬ 
toneum. Again one finds one tibio-condylar articulation 
badly diseased, and the other only slightly affected. Often 
of course the whole knee joint is equally involved. 

The joint cavity may be filled with a clear serous, a 
hemorrhagic, a turbid, or a flocculent fluid, or it may con¬ 
tain the so-called tuberculous pus. In the last case, the 
joint cavity constitutes a cold abscess. There is usually 
nothing characteristic about the appearance of the fluid in 
a tuberculous joint, unless it happen to be turbid and floc¬ 
culent. This is practically pathognomonic. In some 

295 


290 


INFLAMMATION IN BONES AND JOINTS 



Fig. 93. —Old tuberculosis of the knee-joint. The heavy shadows in the plate are not to be 
interpreted as new bone, but as collections of calcified material. Note the decrease in the 
light zone between the bones, showing the disappearance of the articular cartilages. 

cases the joint contains no fluid at all. These are usually 
the slow, dry cases. In these the joint cavity may be ab¬ 
sent, and the bone ends may be bound tightly together by 




TUBERCULOSIS OF THE KNEE 


297 


fibrous adhesions, which run not only from bone to bone, 
but also from each bone to the capsule. When these adhe¬ 
sions are torn apart at operation they leave the bones with 
an irregular, tom, disorganized appearance, that is al¬ 
most diagnostic. 

In some cases the synovial membrane is thickened, 

villous and succulent, giving a boggy, doughy feel to the 

articulation. These usually contain a little free fluid, not 

•/ 

always capable of detection clinically. 

In the cases with free fluid, the patella floats; in the 
boggy cases, it can be moved with a sort of soft resistance; 
in the fibrous it is usually bound tightly down to the 
femoral condyles. 

The ends of the femur and of the tibia often appear to 
he enlarged, but they never are. The swelling is in the 
circumarticular tissues. This swelling, in the cases with 
much proliferation in the synovial membrane, takes on a 
peculiar spindle shape, accentuated by the atrophy of the 
thigh and calf, and the skin, with veins dilated, becomes 
blanched, giving to the joint an appearance from which 
the disease derived its former name of “tumor albus” or 
“white swelling.” The same thing is seen sometimes in 
the elbow, less often in the ankle, and rarely in the 
other joints. 

The knee is held in slight flexion, and the flexors, work¬ 
ing at an advantage over the large extensor, subluxate the 
tibia backward, at the same time rotating it outward. The 
posterior portion of the capsule shrinks after a while, if 
the subluxation is permitted to remain, and prevents the 
return of the tibial head to its place under the condyles. 
If force he employed in the attempt to reduce the subluxa¬ 
tion, the tibial head is levered backward, and possibly one 


298 INFLAMMATION IN BONES AND JOINTS 

of the soft bones may be fractured. This subluxation is 
perhaps most prominent in the cases with marked involve¬ 
ment of the quadriceps pouch, and in mild synovial cases 
is not to be looked for. 

Atrophy of the muscles of the thigh and calf is an early 
and constant phenomenon, especially in the bony type of 
the disease. In this atrophy the bones of the thigh and 
leg take part. 

SYMPTOMATOLOGY 

The disease begins with pain in the knee, stiffness and 
a feeling of discomfort. The patient limps. Swelling 
usually appears early. The swelling may be fluctuating 
or boggy, the patella may float or it may not. In the late 
stages of the disease the mobility of the patella is almost 
always impaired. The knee is in flexion, and its range 
of flexion and extension is limited. Sometimes the patient 
walks upon the toes of the aff ected foot. The flexion in the 
later stages may reach an extreme degree, and, with the 
peculiar outward rotation and general appearance of 
the joint, may make the identification of the disease an easy 
matter. In some cases however the patient may present 
a slightly swollen, painful joint, with nothing character¬ 
istic about it. 

Sensitiveness to pressure of the synovial membrane is 
usually present, best detected when the knee is in flexion. 

Abscess formation is fairly frequent, and, on account 
of the nearness of the joint to the surface, rupture of the 
abscess and secondary infection are hard to avoid. Luck¬ 
ily an infected abscess in a joint that is near to the surface 
is not as a rule so hard to heal as one in a deeper joint, 
like the spine and hip. 


TUBERCULOSIS OF THE KNEE 


299 


PROGNOSIS 

There seems to be a rather definite opinion that the 
prognosis in knee joint disease is better than in tuberculosis 
of other joints, and I believe this is correct, and that it is 
correct because the knee is easier to stiffen. Perhaps, on 
the other hand, it is because mechanical conditions make 
splinting more effectual. 

Conservative treatment requires two or three years at 
best, and under it children sometimes recover with a fair 
degree of motion, though always with the danger of a 
relapse threatening them, as with tuberculosis of any other 
organ. Some good authorities assert that the synovial form 
in adults often recovers with good function, but usually 
when good motion results, one views one’s diagnosis with 
scepticism. At best, under conservative treatment, in the 
adult one looks for a painless, stiff joint, and to attain 
this long continued treatment is necessary. The resulting 
ankylosis is fibrous. Unless a secondary infection has 
been added, bony ankylosis is rare, if it ever occurs. 

Under properly planned radical treatment, the disease 
can be brought to a standstill in about six months. Some 
patients, however, seem to possess no resistance to the 
disease. In them, in spite of treatment, the disease stead¬ 
ily advances, the operative wound breaks down, and a 
thigh amputation must be done to save the patient’s life. 
We see the same thing here as in pulmonary tuberculosis, 
but in this case we have a life-saving measure which we 
do not possess in that. 

TREATMENT 

Some surgeons recommend conservative treatment in 
patients of all ages, some radical in them all, but the trend 
of modern treatment, in which I heartily concur, is toward 


300 


INFLAMMATION IN BONES AND JOINTS 


invariable conservative treatment in children, and invari¬ 
able radical treatment in adults, as soon as a positive 
diagnosis is made. When we speak of a positive diagnosis 
we do not mean one that is made after a rapid examination, 
however experienced the examiner may be, hut one founded 
on indisputable evidence. On the other hand, if physical 
examination, backed by the evidence accorded by the Ront- 
gen rays, shows that the joint is so badly damaged as to 
be incapable of good function, whatever the exact nature 
of the disease may be, positive proof of the presence of the 
tubercle bacillus is unnecessary, and we proceed to com¬ 
plete the task which nature has set for herself, and destroy 
the joint. 

A completely ankylosed, painless joint is better than 
a partially ankylosed, painful one, and far safer. There 
is little hope that this method of treatment will ever become 
very popular among the laity. The usual adult will 
resort to the surgeon who will promise him something bet¬ 
ter, but sooner or later he must submit to the inevitable. 

In spite of the claims that have been made for conserv¬ 
ative treatment in children, if conditions were the same 
in them as in adults we should probably be tempted to 
adopt radical measures, and spare them the long, tedious 
and uncertain course of conservative treatment, but in 
the knee, especially, radical treatment is to be shunned at 
all costs. Here are located two of the most important 
centres of bony growth in the body, and here unsightly 
postoperative deformity is notoriously difficult to avoid. 
Again, radical treatment is not followed by the almost 
certain cure that follows it in the adult. If mv theory, 
whose truth has not yet been completely demonstrated, is 
correct, this is because lymphoid marrow is present in the 
shafts as well as in the ends of the bones, and its presence 


TUBERCULOSIS OF THE KNEE 


301 


is not dependent upon function. Resection does not 
cause its disappearance. 

In spite of all that has been said for many years against 
the radical treatment of tuberculous knees in children, 
its sporadic advocacy is perennial, and evidently cannot 
be killed. Only the opportunity to see, years afterward, 
the results of their treatment, causes its advocates to aban¬ 
don it, and their experience seems powerless to deter 
their successors. 

In this connection it may be said that Hibbs maintains 
that his ankylosing operation does not disturb the centres 
of growth, and hence does not cause shortening. 

CONSERVATIVE TREATMENT 

Precedent to the application of permanent apparatus, 
any deformity in the nature of fixed flexion should be 
corrected, and this may require patience, care and some 
skill. Not only the hamstrings are contracted, but also 
the posterior and lateral ligaments of the joint, and, if 
the tibia be simply straightened by direct force, its 
head will he levered backward with the lateral ligaments 
as a sort of fulcrum, perhaps fracturing the softened 
bone, and the tibia will be brought into a line parallel with 
that of the femur, but on a plane posterior to it. 

Various expedients have been devised to correct the 
deformity. Bilroth recommended two lateral hinges with 
long iron bars whose ends are provided with perforated 
pieces of tin for incorporation in plaster of Paris. The 
limb is put up in plaster piled quite thick in the popliteal 
space. When the plaster has set, it is divided at the knee 
joint, and a wooden wedge is driven in the crack posteri¬ 
orly, forcing it somewhat open. From time to time other 


302 INFLAMMATION IN BONES AND JOINTS 

larger wedges are driven in, until the leg is straightened. 
Several jdaster dressings may be necessary. 

The patient may be put to bed, perhaps with his leg 
in plaster, and then the leg may be put in a sling, and 
traction forward may be made on its proximal part by 
means of weight and pulley from a bar over the bed. 
The weight of the foot and of the distal part of the leg, 
tends to stretch the contracted ligaments, and to lever the 
tibia! head out from under the femoral condyles. 

No marked flexion deformity at the knee should ever 
be corrected too rapidly and forcibly, on account of the 
danger of rupturing the popliteal vessels. Gangrene has 
been caused by rough manipulation. 

After the reduction of the deformity, the surgeon 
will have the choice of plaster of Paris or a brace. It 
is hard to say which is better. Some prefer one, some the 
other. Some employ both. If plaster be chosen, the knee 
should be fairly well, but not excessively, jiadded over a 
well fitting stockinette, and a little padding should be 
applied about the malleoli, and the proximal end of the 
thigh. The shape of the limb, that of an inverted pyra¬ 
mid, must be borne in mind, and the plaster must be molded 
carefully about the knee and calf to prevent it from sag¬ 
ging. At the knee the plaster should be less than of 
an inch thick, and elsewhere less than half that. The 
lighter the plaster is, consistent with strength, the less 
tendency it will ha\ e to sag. It is grotesque to see some 
plastei di essings put on to immobilize the knee, and reach¬ 
ing perhaps five or six inches above and below it. They 
should reach from the perineum to a line about one inch 
proximal to the tip of the lateral malleolus. 

The Thomas Brace.— If the surgeon elect a brace, he 
will probably find that the Thomas brace will serve his 


TUBERCULOSIS OF THE KNEE 303 

purpose better than any other. It is one of the most use¬ 
ful braces that ever has been invented, and consists of a 
padded leather covered steel ring whose outline is that of 
a cross section of the proximal end of the thigh, and of 
two steel rods, running distal from the medial and lateral 
aspects of the ring. At their distal ends these steel rods 
are joined by a rubber shod sole piece. Two broad leather 
bands are provided to support the back of 
the thigh and calf, and the knee is held 
securely in place by a bandage, or by 
another broad leather band, which buckles 
over the front of the joint. Extension is fur¬ 
nished by straps fastened below to the foot 
piece, and running upward to buckles 
attached to adhesive straps on the leg. 

In measuring for the ring, about an inch 
should be allowed for the padding. The 
uprights are the length of the limb from 
perineum to sole, plus about two inches, so 
that the foot will be swung clear of the 
ground. The sole of the other shoe must be raised an 
equal amount to compensate. In the later stages of the dis¬ 
ease when traction is no longer necessary, and in the early 
stages as well, if we believe that fixation only is required, 
the uprights are fastened below to the sole of the shoe, and 
the high shoe on the other side is dispensed with. In any 
case, of course, the brace must be worn night and day. 

When all active symptoms have subsided, and when 
the joint seems well, whatever appliance the patient has 
worn should not be abandoned, but should be left off at 
first during the night, and then by degrees during the day. 
If there be any return of active symptoms, or any tendency 
to deformity, continuous treatment should be resumed. 



Fig. 94. —The Thomas 
knee splint. 
















304 


INFLAMMATION IN BONES AND JOINTS 


Tuberculous knees that have healed in a faulty position 
of fixed flexion, may be straightened by linear osteotomy, 
or better yet by the removal of a wedge shaped piece of 
bone with its base forward. Osgood has devised a very 
ingenious operation for the correction of this deformity . 1 

OPERATIVE TREATMENT 

In operating on a tuberculous knee, the surgeon is 
guided by one of two principles; either he removes as 

much as possible of the tuberculous 
bone and synovial membrane, or he 
disregards completely the extent of 
the disease, and simply strives to 
produce a bony ankylosis. From 
reasons heretofore set forth at 
length, I regard the latter procedure 
as correct. In either case, or with 
whatsoever theory the surgeon oper¬ 
ates, if he succeed in producing a 
bony ankylosis and in avoiding a 
secondary infection, he will cure the 
disease. The knee is an easy joint 
to ankylose: it is therefore an easy 
joint to cure. 

The approach to the knee is 
simple. The incision most often em¬ 
ployed is a curved anterior, trans¬ 
verse one, convex distally, between the condyles, dividing 
the patellar tendon. Some surgeons make the incision 
with the convexity proximal, dividing the quadriceps ten¬ 
don just proximal to the patella. Some employ a straight 
incision, dividing the patella transversely with a saw. 

1 Osgood, R. B.: “A method of osteotomy of the lower end of the femur 
in cases of permanent flexion of the knee joint.” Amer. J. Orth. Surg., 1913, 
xi., 336. 



Fig. 95.—The ring of a left Thomas 
knee splint. C, B, the anterior 
portion, A, B; the perineal portion. 








TUBERCULOSIS OF THE KNEE 


305 


From this point the procedure varies with the surgeon's 

purpose. II he wishes to remove all the tuberculous tissue 

possible, he proceeds to a thorough dissection of all the 

synovial membrane he can reach, and to the removal of all 

the bone patently diseased. If his purpose is simply to 

ankylose, he flexes the knee acutely, dissects the soft tissues 

from the top of the head of the tibia, 

causes his assistant to retract the tissues 

from the head of the tibia and from the 

condyles of the femur, and saws off a 

thin slice from the head of each bone . 2,3 

In order to make the ankylosis more 

•/ 

secure Hibbs 3 4 denudes the sides and 
back of the patella, and hooks it into 
a cavity gouged out of the head of the 
tibia, and the distal end of the femur. 

If fixed flexion was present before the 
operation, and if a portion at least of 
the lateral ligaments be spared, the 
joint locks fast when it is straightened. F ig. oe.-incisjons for o P en- 

-i r> • -i . 1 ing the knee joint. A, B, 

Deep and superficial sutures close the anterior longitudinal in¬ 
cision; C, D, the transverse 

tile wound. incision; E, F, the Jones in¬ 

cision for removal of the torn 

The end of the bones is usually sawn piece of the medial meniscu8 - 

off square. The operator plans his saw cut so that when 
he brings the bone ends together, the bones will be in a 
straight line or slightly flexed as he wishes, and bowed 
neither in nor out. 

The difficulty of getting the two flat bone surfaces 
together, and keeping them in apposition, prompts some 

3 Ely. Leonard W.: “Die Tuberkulose des erwachsenen Kniegelenks, 
etc.” Berl. klin. Woch., 1910, xlvii, 2062. 

3 Ely, Leonard W.: “Tuberculosis of tbe adult knee joint, etc." Trans. 
Sure/. Sect. A. M. A., 1910, 36. 

4 Hibbs, R. A.: “Tuberculosis of tbe knee joint in tbe adult, etc.” N. Y. 
Med. J., 1917, cv, 922. 



20 




30C> INFLAMMATION IN BONES AND JOINTS 

surgeons to practise the Fenwick operation, in which the 
distal end of the femur is sawn convex from before back¬ 
ward and the end of the tibia concave. This operation 
avoids one difficulty, and incurs another, and probably 
greater one. It leaves the bone ends in the very best pos¬ 
sible shape for the formation of a new joint, which is just 
what we wish to avoid. 

Some operators wire the bones together with silver, 
others spike or plate them. Albee recommends a bone 
graft. Other things being equal, metal should not be bur¬ 
ied in the wound, on account of the danger of subsequent 
secondary infection. I have seen infection occur about 
an old spike that had been in for months, and then lost 
the patient eventually, after a thigh amputation. 

After the wound has been sutured and dressed, the 
limb is encased in plaster of Paris from perineum to toes. 
Including the foot is wont to make the pain less. In a 
week or two the plaster may be removed from below the 
malleoli. The limb should be immobilized for about six 
months. Bony union does not take place for about 
one year. 


REFERENCES 


TUBERCULOSIS OF THE KNEE 

Branded Max: “ Uber das Endresultat radikal operierter Kniegelenkstuber- 
kulosen im Kindesalter ” Deut. Ztschr. f. Chir., 1912, cxvii, 490. 

Dollinger, Julius: “Das Zuriickbleiben im Wachsthume der kranken Ex¬ 
tremist bei tuberkulosen Kniegelenksentziindung.” Cent f Chir 1888 
xv, 897. 

Draxdt, M.: “Zur Behandlung der Kniegelenkstuberkulose mit besonderer 
Beriicksichtigung der Resektion.” Beitr. z. klin. Chir., 1905, xlvii, 787. 

Els, Heinrich : “ Ueber die Behandlung der Tuberkulose des Kniegelenks 
und ihre Erfolge.” Beitr. z. klin. Chir., 1 913, lxxxvii, 51. 

Garnier, P. : “Beitrag zur chirurgischen und konservativen Behandlung der 
Gonitis tulierkulosa.” Deut. Ztschr. f. Chir., 1915, cxxxiv, 195. 


TUBERCULOSIS OF THE KNEE 307 

Heinleins: “ Kniegelenkstuberkulose: vollstoendige Luxation.” Munch, med. 
Wchnschr., 1911, lviii, 2308. 

Henderson, M. S.: “ Resection of the knee-joint for tuberculosis.” J. A. M. A., 
1915, lxiv, 140. 

Hibbs, Russell A.: Tuberculosis of the knee-joint in the adult in which 
operations were done eliminating motion by producing fusion of the 
femur and tibia.” N. Y. Med. Jour., 1917, cv, 922. 

Koenig, k.: “Die specielle Tuberkulose der Knochen und Gelenke, 1. das 
Kniegelenk.” Berlin, 1896, Verlag von August Hirschwald. 

• • 

Konig: “ Bemerkungen zur Behandlung der Tuberkulose des Kniegelenks, 
u. s. w.” Arch. f. klin. Chir., 1895, i, 417. 

Leusden, Friedrich Pels: “ Ueber die bei Tuberkulose des Kniegelenkes zu 
beobacktenden Wachsthumsveranderungen am Femur.” Deut Ztschr. f. 
Chir., 1899, li, 257. 

Lin iiart. A.: “ Beitrag zur Resektion des tuberkulosen Kniegelenkes.” Beitr. 
z. klin. Chir., 1909, lxl. 455. 

May, Walter Andreas: “ Leber das Endresultat radikal operierter Knieg- 
elenks-tuberkulosen bei Erwachsenen.” Leipz., 1913, A. C. W. Vogel. 

Sever, J. W., and Fiske, E. W.: “Tuberculosis of the knee-joint in childhood.” 
Am. Jour. Orth. Surg., 1914-1915, xii, 597. 

Schitlowsky, M.: “Beitrag zur chirurgischen und konservativen Behandlung 
der Gonitis tuberkulosa.” Deut. Ztschr. f. Chir., 1915, cxxxiv, 242. 


CHAPTER IV 


TUBERCULOSIS OF THE ANKLE AND TARSUS 

Tuberculosis of the large joints of the extremities is 
peculiar in that it shows no tendency to spread from the 
joint where it originates, through the bone, to the joint at 
its other end. In other words, it remains indefinitely in 
and about the original joint. Tuberculosis of the joints 
of the ankle, tarsus and carpus does not share this peculi¬ 
arity. A focus in one bone may give rise to an infection 
of any joint of which that bone is a component. There¬ 
after the disease may spread to the other bone or bones 
making up that joint, and then to the other bones and 
joints of the region. It is this peculiarity which has made 
tuberculosis of the carpus and tarsus so difficult to treat. 
Its prognosis always has been bad. On the other hand 
the clinical fact has been noted that tuberculosis of the ankle 
has not a great tendency to spread to the other tarsal joints, 
and that disease of the calcaneus usually remains in the bone 
marrow, and does not spread to a joint unless a way is 
opened to it by unwise surgical procedure. 

THE ANKLE 

Tuberculosis of the ankle is much less frequent than 
tuberculosis of the spine, hip or knee, and this comparative 
infrequency has been adduced as an argument against the 
traumatic origin of joint tuberculosis, for the ankle is 
exposed to trauma more than almost any joint in the body. 
The relative frequency of the disease is said to be greater 
in adults than in children, like disease of the smaller joints 
in general, but this is open to question. 

308 


TUBERCULOSIS OF THE ANKLE AND TARSUS 309 

As with other tuberculous joints, the proportion of per¬ 
sons afflicted shows a slight majority in favor of the male 
sex, but not enough to correspond to the greater liability 
to trauma. 

According to Sever , 1 out of 7474 cases of bone and 
joint tuberculosis at the Children’s Hospital, Boston, only 
213 were tuberculous ankles. Of these the right ankle 
was involved in 108 , the left in 90 , and both ankles in 15 . 

Pathology.— The primary focus is said to he located 
most often in the talus, but may be in the tibia, or in the 
fibula. A synovial focus is assumed in some cases. The 
disease may spread through, the talus, and involving one 
of the tarsal synovial membranes, may then attack the 
other tarsal bones, but, as has been said, this phenomenon 
probably is rather rare. 

Abscess formation is the rule in disease in this locality, 
and, because of the nearness of the joint to the surface, 
secondary infection is almost impossible to avoid. 

The condition of “fatty osteomalacia” is seen often in 
disease of the tarsal bones. They cut easily with the knife, 
and are little else but shells. 

Symptomatology. —Pain, swelling and limp, are early 
symptoms, and muscular spasm, limitation of motion, and 
atrophy of the leg muscles are early physical signs. The 
normal contour of the ankle is obliterated, the hollows 
behind and in front of the malleoli, and distal to them dis¬ 
appear, and the whole region becomes diffusely swollen. 
The swelling often assumes the classic spindle shape. The 
foot is usually held in equinus, and the patient walks upon 
his toes, with his knee semiflexed. Sensitiveness to pres- 

1 Sever, J. W.: “Tuberculosis of the ankle joint and tarsus.” Jour. 
A. M .A., 1910, lv, 2128. 







310 


INFLAMMATION IN BONES AND JOINTS 


sure is wont to be pronounced, perhaps localized more or 
less over the place of greatest involvement. 

Differential Diagnosis. —This is made on the gen¬ 
eral principles already set forth, and, with the exercise of 
reasonable diligence and care, rarely occasions much diffi¬ 
culty. A sprained ankle has the traumatic history, with 
the symptoms following immediately, and sensitiveness 
distal to the lateral malleolus. Fractures have the distinct 
traumatic history, with positive X-ray findings. 

Prognosis. —This is not particularly good. Children 
often recover with a stiff joint after secondary infection. 
Resection gives a useful foot in adults, but in them second¬ 
ary infection usually spells amputation. 

Treatment. —Conservative treatment usually gives 
good results in children, and is not difficult to carry out. 
Its duration is shorter than that of disease of the hip 
and knee. 

The joint should be immobilized in a position of adduc¬ 
tion and right angle flexion, by a plaster of Paris dressing 
reaching from the bend of the knee to the toes. If sinuses 
be present, windows may be cut in the plaster at their 
openings. 

If the patient walk directly upon this dressing, he 
will soon break the plaster to pieces, therefore we are com¬ 
pelled to adopt stilting in addition. This is best done with 
the Thomas brace, and a high shoe on the other side. Inas¬ 
much as extension with adhesive straps is impossible in 
disease of the ankle, the brace is slung from the shoulders, 
by a looped strap, which attaches in front and behind to 
the thigh ring. 

The Bier treatment by passive congestion, and helio¬ 
therapy are still recommended abroad particularly. They 
seem especially indicated in the treatment of the ankle, 


TUBERCULOSIS OF THE ANKLE AND TARSUS 311 

tarsus and wrist. Cutting operations are rarely advisable 
upon children’s ankles. 

Operative Treatment.— On acount of the marked 
tendency to abscess formation, with the risk of extension 
to the other tarsal joints, in disease of the ankle joint, 
operative measures should be undertaken in the adult as 
soon as a positive diagnosis is made, and here, even less 
than in most other localities, should one attempt the futile 
operation of scraping and pack¬ 
ing. To do this is to invite dis¬ 
aster, for, if the disease once 
spread through the talus into the 
tarsal synovial cavities, an exten¬ 
sive resection, or more probably 
an amputation, almost always 
will be necessary. Our object is 
to produce a bony ankylosis, but 
this is extremely difficult in the 

* Fig. 97.—Whitman’s incision for exci- 

ankle. Usually all we can secure sion of the talus 

is a fibrous one. Theoretically a bone dowel, driven 
up from the sole, through the talus, into the tibia, should 
answer the purpose well. 

The operation that has given the best results is ablation 
of the talus, with removal of the joint surfaces of the bones 
with which it articulates—the Whitman operation. The 
incision is a curved one with the convexity distal, starting 
proximal to the lateral malleolus, and behind it, and run¬ 
ning distal and forward to the anterior extremity of the 
talus. The peroneal tendons may be divided and later 
sutured. In disarticulating the talus one must keep close 
to the bone on the medial aspect, in order to avoid damag¬ 
ing the vessels passing behind the medial malleolus. If 
the entire foot be subluxated backward, and if the sides 





312 INFLAMMATION IN BONES AND JOINTS 

of the calcaneus be freshened for apposition to the fresh¬ 
ened malleoli, the stability of the result will be increased, 
and a serviceable member will be secured. 

In the adult as well as in the child in secondarily 
infected cases, before resorting to amputation, some 
surgeons believe in a prolonged course of passive hyper- 
a?mia, combined with the use of Klapp’s cupping, and 
heliotherapy. 


THE TARSUS 

1 he joints of the tarsus may be affected primarily, or 
secondarily by extension from the ankle joint, especially 
if the primary focus be situate in the talus. Secondary 
infection with pus producing organisms, and abscess forma¬ 
tion aie the rule, and usually occur early. According to 
Hahn 2 who has compiled statistics of 704 cases of tuber¬ 
culous disease of the foot, the frequency of the disease 
diminishes according to the distance of the affected bone 
from the ankle. 

I he significant point in tarsal disease, besides the 
spongy structure of all the bones, is the extent and the 
i anufications of the synovial membranes. There are six 
°r seven separate synovial cavities. The bones are bound 
together by ligaments running in different directions, and 
these again are covered by tendons, nerves and blood ves¬ 
sels. To ascertain the extent of the disease in the bones 
and synovial membranes is a physical impossibility. To 
attempt to eradicate it without an amputation is difficult. 

I he symptoms and physical signs are the same as in 
tuberculosis of other joints. The patient usually walks 
upon his heel, with his foot abducted to remove it from 

2 Hahn, o.: “ Ueber die Tuberkulose der Knochen und Gelenke des 
busses, u. s. w. Beit. z. klin. Chir., 1900, xxvi, 525. 





TUBERCULOSIS OF THE ANKLE AND TARSUS 313 

strain. Two important points in differentiating the affec¬ 
tion from painful flat foot are the local sensitiveness to 
pressure, and the signs of inflammation over the affected 
region. A skiagram will show roughening of the bone, 
with rarefaction, and irregularity of contour. Kohler’s 7 
disease is also to be remembered. 

Treatment. —In children this is almost invariably 
conservative. The reparative processes are vigorous, and 



Fig. 98. Tuberculosis of the tarsus. Talo-navicular joint laid open. 

Note the irregularity of the articular cartilage. 

a foot with discharging sinuses, which appears to be hope¬ 
lessly diseased, under conservative treatment often recov¬ 
ers and forms a useful member. The temptation to 
operate is strong, but should be stoutly resisted. In cases 
with secondary infection, in which drainage is poor, the foot 
may be immersed in a bath of normal salt solution at a 
temperature of 105°-110 F., for an hour or two daily. In 
adults, as well as in children, heliotherapy and passive 
hyperemia, supplemented by the employment of Klapp’s 
cups, may be given a faithful trial, though I am sceptical 
of the results in adults, and personally should not advise 
the treatment. 





314 INFLAMMATION IN BONES AND JOINTS 

The mechanical treatment is best carried out with some 
such brace as the Thomas, and, if too many sinuses be not 
present, a plaster of Paris dressing in addition. The foot 
should be put up in adduction, at right angle flexion with 
the leg. If, on account of the sinuses, we are unable to 
apply plaster, we may be obliged to permit the foot to 
remain in a faulty attitude until the sinuses are healed. 
Then the faulty attitude may be gradually corrected by 
plaster dressings. 

Operative Treatment. —In tuberculosis of the ankle 
in the adult the treatment, as in disease of other joints, 
is almost always operative. In a very early case, with a 
bone focus and no synovial involvement, an early excision 
might perhaps effect a cure. Later this will be difficult 
or impossible. 

In tuberculosis of the navicular there may be involve¬ 
ment of two synovial cavities, one of them extensive and 
with a number of ramifications; in disease of the cuboid 
there may be involvement of three, in disease of the talus 
or calcaneus, of three. When two or three bones are 
diseased, four, five or six synovial cavities may be involved. 
The disease seems to run riot when once it has become 
diffused through the tarsus, and all temporizing measures 
are usually without avail. 

In uncomplicated cases in the adult, wide resections 
have given fairly good results. Theoretically a bone graft 
laid down right through the diseased region should be the 
ideal tieatment. I have never had the chance to do this 
operation in tuberculosis of the tarsus, but have done it in 
the wrist with excellent results. 3 

3 Ely, Leonard W.: “An operation for tuberculosis of the wrist.” Jour. 
A. M. A., 1920, lxxv, 1707. 






TUBERCULOSIS OF THE ANKLE AND TARSUS 


315 



TUBERCULOSIS OF THE CALCANEUS 


This occurs fairly frequently in children, not so fre¬ 
quently in adults, and is peculiar in several respects. It 
affects, almost invariably, the anterior spongy part of the 



316 


INFLAMMATION IN BONES AND JOINTS 

bone, is characterized by the formation of a sequestrum, 
breaks down early, ruptures on the lateral aspect, and very 
rarely involves a joint. 

The disease is a stubborn one, and its treatment is most 
tedious. If secondary infection have taken place, the 
sequestrum should be removed. The usual measures of 
passive hyperasmia, Ivlapp’s cupping, heliotherapy, etc., 
may be tried, perhaps also plugging the cavity with an 
iodoform paste. Finotti has had good results with the 
operation of ablation of the calcaneus, and says that the 
ability to walk is not seriously compromised. If the ten¬ 
don sheaths are badly involved’ an amputation will prob¬ 
ably be necessary, according to Finotti. 4 

REFERENCES 

TUBERCULOSIS OF THE ANKLE AND TARSUS 

Fixotti. E.: “ Tuberkulose des Calcaneus.” Dent. Ztschr f Chir 1895 
xl, 450. 

Galzix, E.: “ Resection pour tuberculose osseuse.” Rev. de. Chir. 1905 
xxxii, 342. 

Hahx, O.: “Ueber die Tuberkulose der Knochen und Gelenke des Fusses, 
u. s. w.” Beitr. z. klin. Chir., 1900, xxvi, 525. 

Maass: “ Die Tuberkulose des Sprunggelenks.” Arch, f klin Chir 190‘ 7 
lxv. 182. 

Ohse. E.: “Ueber Dauererfolge bei Behandlung der Fusswiirzeltuberkulose 
(lurch Resektion mit vorderem und hinterem Querschnitt.” Beitr - 
klin. Chir., 1908, lvii, 276. 

Rogers, Mark E.: “Prognosis and treatment of tuberculosis of the ankle in 
adults.” Boston Med. Sure/., Jour., 1911, clxiv. 811. 

Sever, James Warren: “Tuberculosis of the ankle-joint and tarsus” J A 
M. A., 1910, lv, 2128. 

Spexgler, E.: “ L eber Fussgelenk-und Fusswiirzel Tuberkulose.” Dent Ztschr 
f. Chir., 1896-1897, xliv, 1. 

Wolff, Oscar: “ Ueber ausgedehnte Resectionen am tuberkulosen Fuss” Arch 
klin. Chir., 1896, liii, 304. 


Fixotti, E.: L eber Tuberkulose des Calcaneus.” Deut. Zeit f Chir 
1895, xl, 450. ' 







CHAPTER V 

TUBERCULOSIS OF THE SHOULDER 

Tuberculosis of the shoulder is rather rare, especially 
so in childhood. Roughly, two clinical forms of the dis¬ 
ease are recognized, one in which there is a production of 
soft granulation tissue, with formation of abscesses, and 
the other in which the slow tuberculous process in the mar¬ 
row eats away, so to speak, the bone in the humeral head, 
and destroys it without abscess. The latter is more fre¬ 
quent, and is known as “caries sicca.” The primary focus 
is usually located in the head of the humerus. In all my 
specimens this aj)pears to have been the case. 

Pain is an early symptom, felt in the shoulder, and 
running down the arm. Limitation of motion is present, 
but, on account of the mobility of the shoulder girdle on 
the sterno-clavicular joint, the limitation may escape the 
patient’s notice for some time. In testing for it, the 
shoulder girdle should be held fast with one hand, while 
the humerus is moved about with the other. If the patient 
is simply directed to move his arm about, the vicarious 
motion at the sterno-clavicular joint may give a false im¬ 
pression to the observer. The chief limitation is in abduc¬ 
tion, and in rotation. 

Atrophy of the deltoid and of the other shoulder mus¬ 
cles, is an early and a very important physical sign, and 
is especially prominent in the dry cases. It gives to the 
shoulder a peculiar flattening. The roundness of the del¬ 
toid disappears, and is replaced by a more angular contour. 
Sensitiveness to pressure is quite marked. Fluctuation 

317 


318 


INFLAMMATION IN BONES AND JOINTS 


may be detected in the moist cases. Abscesses appear at 
the margin of the deltoid muscle, and, rupturing, may 
give rise to stubborn sinuses. 

Besides the other forms of shoulder arthritis of the 
first great type, there are two lesions of this region which 
deserve especial mention, namely, subacromial bursitis and 
acromio-clavicular arthritis. The general principles of the 
differentiation of the other members of this type have 
already been set forth. 

Subacromial, subdeltoid or Duplays bursitis, 1,2> 3) 4 ’ 
“periarthritis” of the shoulder is, as its name implies, an 
inflammation of the bursa, about three centimetres in 
diameter, situated partly beneath the deltoid, partly be¬ 
neath the acromion, and between them and the tendon of 
the supraspinatus muscle. It is often traumatic in origin, 
but often its cause can only be surmised. It is closely 
simulated by lesions of the subjacent supraspinatus ten¬ 
don. The bursa may contain fluid, or its cavity may be 
obliterated by the tight fibrous adhesions which bind 
together its walls. Collections of lime have been described 
in it, but Brickner and others have shown that the lime is 
not in the bursa, but beneath it. 


The symptomatology of subacromial bursitis is similar 
to that of tuberculosis of the shoulder, or identical with it. 
The same pain, sensitiveness, limitation of motion, and 
atrophy are all present. The X-ray plate may show a 

1 Brickner, W. M.: “ Pain in the arm: subdeltoid (subacromial) bursitis” 
J. A. M. A., 1917, lxix, 1237. 

2 Codman, E. A.: “On stiff and painful shoulders” Boston Med. and 
Surg., Jour., 1906, cliv. 613. 

3 Codman, E. A.: “Bursitis subacromialis or periarthritis of the shoulder 
Joint.” Boston Med. and Surg., Jour., 1908, clix, 533. 

4 Codman, E. A.: “Complete rupture of the supraspinatus tendon etc.” 
Boston Med. and Surg., Jour., 1911, clxiv, 708. 






TUBERCULOSIS OF THE SHOULDER 


319 


\ 


shadow corresponding to the location of the bursa, a col¬ 
lection of calcareous material in the same region, a slight 
irregularity at or near the insertion of the supraspinatus 
muscle, or perhaps a small tear of the greater tuberosity. 
Sometimes a distinct history of trauma can be obtained, 
such as a fall upon the shoulder, or an overstrain throwing 
a baseball, with the symptoms following immediately. In 
the absence of definite evidence a positive diagnosis between 
tuberculosis of the shoulder and bursitis is impossible at 
the first examination. If the pain and stiffness continue, 
sooner or later a tuberculous process, if present, will make 
itself known by rarefaction in the humeral head. 

In acromioclavicular arthritis the pain and sensitive¬ 
ness can be localized by careful examination, in the acromio¬ 
clavicular joint, as distinct from the shoulder joint proper. 
Abduction of the arm is limited and painful, but not 
rotation. The X-rays make the positive differentiation. 
The frequency of lesions of this joint is not generally 
appreciated . 5 

Treatment. —In children immobilization may be se¬ 
cured by bandaging the arm to the side, and slinging the 
forearm from the neck. The clothing should be worn 
over the dressing. The author’s brace constitutes a ser¬ 
viceable appliance for the later stages of the disease. 1 ’ 

Bony ankylosis is difficult or impossible to secure by 
operation, but resection usually gives good results, and 
is followed by tight fibrous ankylosis. The arm should be 
put up after the operation on an aeroplane splint, to pre¬ 
vent the disabling adduction that ordinarily follows opera- 

5 Severs, R.: “ Ueber die Bedeutung des Akromialgelenkes, u. s. w.” 
Archiv. f . klin. Chir., 1914, cv, 418. 

«Ely, Leonard W.: “A new brace for the shoulder joint.” Med. News, 
1904, lxxxv, 160. 


'S 





320 INFLAMMATION IN BONES AND JOINTS 

tions on the shoulder. If ankylosis in abduction can be 
secured, the rotation of the scapula will permit excellent 
function in the joint. For the same reason immobiliza¬ 
tion in interna] rotation should be avoided. 

Several operations for resection have been devised. 
The simplest and the best for routine work is perhaps that 
through the anterior incision with the arm in abduction 
on a board. The incision, about twelve centimetres long, 
runs distal from the clavicle along the anterior border of 
the deltoid. The operator identifies the median cephalic 
vein, and retracts it or ties it between ligatures, carries 
his dissection between the deltoid and the pectoralis major, 
anterior to the biceps tendons, to the joint capsule, and 
slits the capsule widely at right angles with the line of the 
joint. He then dissects subperiosteally all the tissues 
from the head and from the tuberosities, the assistant 
rotating the arm meanwhile first in one direction, and then 
in the other. The assistant dislocates the head through 

o 

the wound, and the operator saws it off. If he believe in 
the efficacy of the removal of tuberculous tissue, he removes 
all he can reach with knife, scissors, gouge and chisel; 
otherwise he contents himself with the removal of the head 
and the articular surface of the glenoid. The operator 
finally closes the wound with deep and superficial sutures, 
dresses it, and puts the limb on the splint so applied that, 
when the patient stands, his hand will be about on a level 
with his mouth. The splint should be worn for two or 
three months. 

Rocher s posterior incision offers no particular advan¬ 
tages in tuberculosis of the shoulder, and is much more 
difficult. 


TUBERCULOSIS OF THE SHOULDER 
REFERENCES 

TUBERCULOSIS OF THE SHOULDER 


321 


Duplay: “ Sur une forme particuliere d’osteo-arthrite tuberculeuse de 
l’epaule.” Semairte Med., 1897, xvii, 81. 

Koxig, Wilhelm Victor: “Die Tuberkulose des Schultergelenkes.” Deut. 
Ztschr. f. Chir., 1891-1892, xxxiii, 403. 

Monday, et Audry: “ Les Tuberculoses de l’epaule.” Rev. de Chir., 1892, 
xii, 224. 

Wolff, Oscar: “Tuberkulose im Schultergelenk und Caries des Processus 
coracoideus.'’ Cent. f. Chir., 1898, xxv, 146. 


CHAPTER VI 


TUBERCULOSIS OF THE ELBOW 

The disease is said to begin most often in the ulna, 
less frequently in the humerus, and least frequently in the 
head of the radius. Primary synovial disease seems to be 
fairly common. In one of my specimens the only bone 
lesion discovered was a bunch of tuberculous granulations 
sprouting up through the articular cartilage of the radius. 
Abscess formation is frequent, and bursting of the abscess 
can with difficulty be prevented. 

T he pain is felt in the elbow, and perhaps shoots down 
the forearm. Swelling is an early symptom, and is us¬ 
ually diffuse. If fluid be present, it is manifest posteriorly 
at the sides of the triceps tendon. The muscles of the arm 
and of the forearm shrink, and this atrophy, coupled with 
the swelling of the joint, causes the classic spindle shape 
of the elbow, so often seen in the elbow, knee and ankle. 
On the other hand, swelling may be absent entirely in the 
slow, dry, fibrous cases. 

The forearm is semiflexed, and midway between pro¬ 
nation and supination. All motions in the elbow may be 
limited, or the limitation may be confined to flexion and 
extension, rotation remaining free. In the latter case, the 
radio-humeral pouch is assumed to be intact. 

The differential diagnosis rarely causes much difficulty. 
Leaving out of consideration the general diagnostic points 
already detailed, for some unknown reason a slow, chronic, 
uniarticular lesion in the elbow joint is usually tuberculous. 

Treatment. —Here as in other joints, the treatment 
is conservative in children, radical in adults. 

322 


323 


TUBERCULOSIS OF THE ELBOW 

Conservative Treatment. —Some surgeons put their 
trust in heliotherapy and passive hyper amia, slinging the 
forearm from the neck during the course of the treatment. 
Most surgeons rely upon immobilization in plaster of 
Paris. The elbow is put up in plaster, in flexion at a right 
angle or slightly beyond, and is kept in plaster until it is 
well. This position, enabling the patient to get his hand 
to his face, is the most serviceable for the general run of 
patients, but the rule may be modified in certain circum¬ 
stances. Adults should choose the attitude in which a 
stiff elbow would be most useful to them in their business. 

In order to get the joint into the required position, 
ether or gas may be administered, or, better yet, the method 
of Thomas may be adopted. Thomas slung the wrist to 
the patient’s neck, pulling the sling tight enough to make 
him bend his neck down toward his hand. As this position 
is uncomfortable, the patient gradually straightens up his 
head, flexing his elbow to that extent. This procedure 
is repeated daily until the required flexion has been secured. 

If sinuses be present, windows may be cut in the plaster. 
Carrying the plaster bandage repeatedly up and down the 
extensor surface of the arm and forearm, avoids the piling 
up of the plaster in the reentrant angle, which occurs with 
the ordinary method of application. The dressing reaches 
from the axilla to the wrist, and is reinforced by an ordi¬ 
nary sling about the wrist. 

Operative Treatment. —The operative treatment of 
a tuberculous elbow is not, as a rule, very satisfactory, and 
this is probably because the joint is a difficult one to anky- 
lose. A bony ankylosis in an attitude of right angle 
flexion, would give a serviceable member. The customary 
treatment is resection. This gives a rather loose joint, 
which appears for a time to be well. Then, with re-forma- 


324 


INFLAMMATION IN BONES AND JOINTS 


tion of the synovial membrane, the disease lights up afresh, 
and compels another resection, with the sacrifice of more 
hone. The resection is repeated, perhaps several times, 
until at length, with the ends of the bones sclerosed and 
tied loosely together with fibrous tissue, cure results. A 
flail joint is not very useful. If one expects nature to 
build up an elbow joint anew after a resection, as in Ollier’s 
classic and oftquoted case, one will be disappointed. (See 
the section on bone formation in the first chapter.) 

The resection is done subperiosteally, and the operator 
must beware to keep close to the bone throughout the 
operation, anteriorly especially to avoid the vessels and 
nerves, medially especially to avoid the ulnar nerve as it 
passes behind the medial condyle. Some surgeons employ 
two posterior incisions, some Kocher’s incision, and some 
the Z-shaped incision of Ollier, but most prefer the single, 
long posterior incision. 

The single posterior incision, about twelve to fifteen 
centimetres long, is made over the middle of the olecranon, 
and is carried down to the humerus and ulna, opening the 
joint. The olecranon, the posterior surface of the ulna 
for a short distance distal to it, and the posterior surface of 
the distal end of the humerus are skeletonized. The ole¬ 
cranon process is removed with a few strokes of the mallet 
and chisel, giving access to the joint. After the condyles 
of the humerus and the end of the ulna have been denuded 
of periosteum, they are removed with saw or chisel. The 
head of the radius can be reached through the opening in 
the lateral wall of the wound, and it also should be removed. 
The wound is closed with deep and superficial sutures. 
Some authorities have maintained that if the joint be put 
up in full extension for a week or so, and if the position 


TUBERCULOSIS OF THE ELBOW 


325 

then be changed to right angle flexion, bony ankylosis will 
ensue. The custom is to put it up in flexion. 

There is a good opportunity, in disease of the elbow, for 
the employment of ingenuity to ankylose the joint with 
a bone dowel or inlay graft. At the suggestion of one of 
my students I attempted to drive a dowel through the 
olecranon into the medial condyle, but evidently missed 
the condyle, for motion was present when the plaster was 
removed six weeks later. It might be possible to run a 
strut from the olecranon to a niche just proximal to the 
olecranon fossa of the humerus. Of course, if the radio- 
humeral joint is intact, all ankylosing work should he done 
between the ulna and the humerus, so as not to compromise 
the important motion of rotation. To lay down a graft 
between the head of the radius and the lateral condyle 
should be a comparatively simple matter. 

REFERENCES 

TUBERCULOSIS OF THE ELBOW 

Bardexheuer: “ Zur Frage tier radikalen Friihresektion ties tuberkulosen 
Ellenbogengelenkes iiberhaupt sowie besonders im kindlichen Alter.” 
Deutsche. Ztschr. f. Chir., 1906, lxxxv, 1. 

Damianos, N.: “ Beitrlige zur operativen Behandlung tier Tuberkulose ties 
Ellbogengelenkes.” Deutsche. Ztschr. f. Chir., 1904, lxxi, 288. 

Lossen, W.: “ Beitrlige zur extrakapsularen Radikal-resektion ties tuberku¬ 
losen Ellenbogengelenks.” Deutsche. Ztschr. f. Chir., 1905, xcii, 120. 
Oschmanxj “Ueber die operative Behandlung ties tuberkulosen Ellenbogen¬ 
gelenks und ihre Endresultate.” Arch. f. klin. Chir., 1900, lx, 177 and 397. 
Reiner, Hans: “ L T ber die funktionellen Resultate tier Resektion ties Ell- 
bogengelenks mit Interposition eines Muskellappens nach Helferich.” 
Deutsche. Ztschr. f. Chir., 1910, civ, 209. 

Sever, J. W.: “Tuberculosis of the elbow.” Boat. Med. Surg., Jour., 1910, 
clxii, 666. 

Todd. T. W.: “The end result of excision of the elbow for tuberculosis.” 
Ann, Surg., 1913, lvii, 430. 

Walter: “ Osteo-arthrite tuberculeuse du coude droit, etc." Bull, et Mem. 
Soc. de Chir. de Paris, 1913, xxxix, 1544. 


CHAPTER VII 


TUBERCULOSIS OF THE WRIST 

Tuberculosis of the wrist is rare in childhood, some¬ 
what less so in the adult. The primary focus may be in any 
one of the bones entering into the formation of the joint, or 
possibly in the synovial membrane. The most frequent 
starting place is said to be the head of the radius. Owing 
to the great extent of the synovial membrane, and to its 
many ramifications, the disease, once started, tends to 
spread widely, and to involve the synovial cavities one 
after another in a manner described in the section on 
tuberculosis of the tarsus. Abscesses form early and 
break down, leaving infected sinuses leading down to the 
joint. The tuberculous inflammation is especially likely 
to spread to the tendon sheaths passing over the joint, 
and the resulting tuberculous synovitis adds severity to 
the disease. 

The wrist is often swollen, and usually it is in slight 
flexion and in pronation. Sensitiveness is present over the 
site of the disease, and sometimes fluctuation and muscular 
atrophy. A boggy swelling is more frequent than a fluc¬ 
tuating one. Motion of the joint is restricted in every 
direction, and, as a rule, quite painful. If the tendon 
sheaths £ire involved, the motions of the fingers also 
are restricted. 

In the matter of differential diagnosis only two things 
need particular notice, namely tuberculosis of the tendon 
sheaths, and fracture of one of the carpal bones, most often 
the navicular. 


326 


TUBERCULOSIS OF THE WRIST 


327 


In tuberculous tendovaginitis, the swelling is more 
superficial, in a manner of speaking, and is localized to 
the region of the tendon sheaths. It moves up and down 
with the movement of the fingers. The Ildntgen rays 



Fig. 100. —Tuberculosis of the wrist, treated with plaster of Paris dre»<3“ 
ings for several years. Author’s operation in August 1919. Positive 
guinea pig test with some of the material removed from the joint. 


reveal no disease in the hones of the wrist, and motion at 
the wrist is unrestricted. Essential tuberculosis of the 
tendon sheaths is rare. 

In fracture of the carpal hones, an injury immediately 
antedates the trouble, and the sensitiveness and swelling 
are limited to a particular region. The Rontgen rays show 
the fracture. 


328 


INFLAMMATION IN BONES AND JOINTS 


TREATMENT 

For conservative treatment, the usual expedients are 
employed*—heliotherapy, passive hyperaemia, immobiliza¬ 
tion, etc. Iodoform injections have their advocates here 
as in other joints. If immobilization be chosen, as I think 
it should be invariably in children, the hand should be put 



Fig. 101. The wrist shown in Fig. 100, eleven months after opera¬ 
tion. Apparent cure with a stiff wrist. 


up in a position of slight superextension. This attitude 
gives the best function. . The plaster reaches from the 
bend of the elbow to the metacarpophalangeal joints, and 
is cut out well at the base of the thumb. Free motion 
in tlie fingers and thumb is to be encouraged. The 
prospects of a cure by conservative measures are not 
particularly bright. 

Operative treatment heretofore has also been disap¬ 
pointing in disease of the wrist. One resection follows 




TUBERCULOSIS OF THE WRIST 


329 

another, until at last the joint becomes secondarily infected, 
and an amputation is necessary to save the patient s life. 
The only good results seemed to follow wide resection, 
with removal of all the carpal hones, the end of the radius, 
and the bases of the metacarpals. I have employed the 
following operation in two cases with beautiful results, 
and recommend it strongly. It has a strong theoretical 
foundation, and the 
results indicate that 
the theory is correct . 1 

The longitudinal, 
median, posterior in¬ 
cision, about fifteen 
centimetres long, runs 
from a point about five 
centimetres proximal 
to the end of the radius 
to one about five cen¬ 
timetres distal to the 
proximal end of the 
third metacarpal. The 
incision is deepened, 
and the extensor ten¬ 
dons are retracted. 

The periosteum over 
the distal end of the 
radius, and the proximal end of the metacarpal is incised 
longitudinally for about two centimetres, and pushed 
aside, baring the bones. With a motor saw a gully about 
five millimetres wide is cut in the wrist, running into 
the third metacarpal and the radius for the distance of one 

1 Ely, Leonard W.: “An operation for tuberculosis of the wrist.” Jour. 
A. M. A., 1920, Ixxv, 1707. 



Fig. 102.—Author’s operation with bone graft for tubercu¬ 
losis of the wrist. 












330 


INFLAMMATION IN BONES AND JOINTS 


centimetre. The gully is cut quite superficial in the carpal 
bones but deep in the radius and metacarpal. A graft 
about three centimetres long and five millimetres wide, 
with periosteum attached, is then removed from the antero¬ 
medial cortex of the tibia, and is fitted into the gully. 
When the hand is forced into superextension the graft locks 
fast. Deep and superficial sutures close the wound. The 
hand is put up in plaster of Paris, while care is taken to 
maintain the superextension. After the plaster has par¬ 
tially set, it is slit up longitudinally together with every 
turn of the bandage underneath, for the postoperative 
swelling is considerable. The fingers and thumb are left 
free, and early motion of them is enjoined. The plaster 
stays on for three or four months, so as to give time for 
the formation of a firm bony bridge between the radius 
and the metacarpal. 


REFERENCES 

TUBERCULOSIS OF THE WRIST 

Brigel, O.: “Die Jodoformbehandlung der Handgelenktuberkulose und ihre 
Dauerresultate.” Beitr. z. klin. Chir., 1898, xx, 1. 

Deutschlander, Carl: “Die isolierte Tuberkulose des Os naviculare carpi, 
zugleich ein Beitrag zur Genese der Handgelenkstuberkulose.” Fortschr. 
a. d. Geb. d. Rontgenstrahlen, 1911-1912, xviii, 264. 

Ely, Leoxard W.: “An operation for tuberculosis of the wrist.” J. A. 3/. A ., 
1920, lxxv. 1707. 

Girard, M. L.: “La Tuberculose du Poignet chez l’enfant.” Theses de Paris. 
1908-1909, xvii. 

Wolff, Oscar: “Zur Resection des tuberkulosen Handgelenks.” Arch. f. klin. 
Chir., 1896, liii, 312. 


CHAPTER VIII 


TUBERCULOSIS OF THE SACRO-ILIAC JOINT 

Tuberculosis of this joint is very rare. Its occur¬ 
rence in childhood is unknown. The male sex is said to 
claim a small majority of the patients, and among women 
the affection is especially apt to occur during pregnancy. 

The synovial membrane is comparatively small in 
extent, but the great masses of cancellous bone on either 
side of the joint afford the disease a good field for exten¬ 
sion. The ligaments above and below are strong and thick, 
but those in front and back are thinner, and through these 
the abscess, whose formation is the rule in disease of this 
joint, may break anteriorly into the pelvis, or posteriorly, 
or both anteriorly and posteriorly. Of fifty-nine abscesses 
tabulated by Van Hook 1 twenty-one, or 38.2 per cent, 
were extrapelvic, and thirty-eight, or 61 per cent, were 
intrapelvic. Secondary infection of the abscess almost 
always takes jilace, and, when it occurs, the disease has a 
free field in the sacrum and ilium, giving rise to many bur¬ 
rowing sinuses and to marked constitutional involvement. 

Pam is the first symptom of which the patient com¬ 
plains, felt either at the seat of the disease, or in the but¬ 
tock, or shooting down the lower extremity. It is wont 
to manifest itself as a severe sciatica, and to be increased 
by motion, that is, by walking, coughing or sneezing. It 
can be brought out by pressing the wings of the ilia 
together, or by the Kernig manipulation. 

On account of the pain the patient stands with his 

1 Van Hook, W.: “Tuberculosis of the sacro-iliac joint.” Annals of Surg., 
1888, viii, 407; 1889, ix, 35 and 115. 


331 






332 INFLAMMATION IN BONES AND JOINTS 

weight thrown over on the sound leg, giving a pronounced 
lateral curvature to the spine. The Kernig sign is posi¬ 
tive. Swelling, on account of the nearness of the joint to 
the surface, appears early. Local sensitiveness to pres¬ 
sure can be detected posteriorly, or anteriorly in the vagina 
or rectum. The fluctuation of an abscess can be felt in 
either one of these places or in both. 

The prognosis has been distinctly bad. Owing to the 
superficial situation of the disease the abscess is extremely 
liable to early infection, and infection here usually means 
death. There is almost no limit to the extension of the 
disease through the pelvic bones, and the sinuses burrow in 
every direction. 

The treatment always has been unsatisfactory. Text¬ 
books pass over it rather cursorily, and necessarily so. 
One sees so few cases, even in a large clinical experience, 
that one hardly has a chance to formulate any well 
defined method. 

Not much is to be expected from conservative meas¬ 
ures. Whitman recommends a plaster spica, or a double 
Thomas hip splint combined with crutches. A high shoe 
should be worn on the well side so as to relieve the affected 
joint from weight hearing. 

Operative Treatment.— Until recently the outlook 
after operation on a tuberculous sacro-iliac joint was decid¬ 
edly gloomy, and in probably no joint was the error of the 
old theory of operating more clearly demonstrated. The 
surgeon, attempting to remove all the diseased tissue, of 
course failed. The wound broke down, became infected, 
and death usually was not long delayed. Recent results, 
based solely on the theory of building a bony bridge 
across between the ilium and the sacrum, have been 
more successful. 


TUBERCULOSIS OF THE SACRO ILIAC JOINT 333 


Hibbs 2 makes a curved incision along the posterior 
third of the iliac crest, continued down over the sacro-iliac 
joint, and reflects the thick flap of skin and subcutaneous 
tissues. He then chisels a large bone flap from each bone, 



Fig. 103. —The Smith-Peterson approach. 
The dotted line represents the incision in 
its relation to the ilium; the curved limb of 
the incision extends from the posterior supe¬ 
rior spine two-thirds of the distance to the 
anterior superior spine. The straight limb 
runs from the posterior superior spine in 
the direction of the fibres of the igluteus 
maximus muscles for a distance of approx¬ 
imately three to four inches. 



and turns it over on the denuded surface of the other. 
The iliac flap includes the external lamella of the posterior 
part of the ilium with most of the posterior superior 
spine and the attached periosteum and soft tissues. The 

2 This description is from a personal communication of Doctor Hibbs. 
The operation has not been published as yet. 












334 


INFLAMMATION IN BONES AND JOINTS 



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TUBERCULOSIS OF THE SACRO ILIAC JOINT 335 

sacral flap includes the external 
lamella of the proximal, lateral 
part of the sacrum, with its peri¬ 
osteum and attached soft tissues. 

Albee employs a bone graft 
between the sacrum and ilium. 

Smith-Peterson has recently 
devised an extremely ingenious 
method of approach to the joint. 

H is incision has two arms, one run- 



Fig. 107.—Window removed 
from ilium down to the 
sacro-iliac joint. 



Fig. 108. —Cortex removed 
from portion of the sacrum 
opening the cancellous bone. 


ning from the posterior superior 
spine of the ilium, along the crest 
for about fifteen centimetres. It 
is carried down to the bone. The 
other arm runs from the posterior 
superior spine distally and ante¬ 
riorly in the direction of the pos¬ 
terior inferior spine toward the 
saero-sciatic foramen for about 
fifteen centimetres. This arm is 


carried down to the bone, splitting 
the fibres of the gluteus maximus, 
in whose direction it runs. The 
thick flap of skin, fascia, periosteum 
and muscle is then reflected distally 
and anteriorly, the fibres of the 
gluteus maximus and medius being 
separated from the bone close to 
their origin from the ilium. This 
procedure lays bare the whole 
posterior portion of the external surface of the ilium. 

The operator then removes from the ilium at a place 
corresponding to the location of the distal part of the 



Fig. 109.—The block of bone 
from the ilium countersunk into 
the sacrum. 






336 


INFLAMMATION IN BONES AND JOINTS 


sacroiliac joint, a bony block about 1x3 centimetres in 
diameter right down to the sacro-iliac joint. The ilium 
here is often very thick. Next he goes through the sacro¬ 
iliac joint, and removes a corresponding piece of bone 
from the sacrum. Now he countersinks his block of iliac 
bone into the hole, so that it passes through the joint into 
the sacrum. The wound is closed, and a double plaster 
of Paris spica is applied for two months, then a single spica. 

REFERENCES 

TUBERCULOSIS OF THE SACRO-ILIAC JOINT 

Codivilla, Alessandro: “ Sulla cura della tuberculosi sacro-iliaca.” Bologna, 
L. Cappelli, 1917. 

Naz: “ De l’arthrite tuberculeuse sacro-iliaque etc.” These de Paris, G. 
Stemheil, 1897. 

Poore, Charles T.: “Disease of tbe sacro-iliac synchondrosis.” Am. Jour. Med. 
Sci., 1871, i, 62. 

_ • 

Bidlon, John and Jones, Robert: “Disease in the sacro-iliac articulation.” 
Ann. Surg., 1893, xvii, 285. 

Van Hook, Weller: “Tuberculosis of the sacro-iliac joint.” Ann. Surg., 
1888, viii, 401 and Ann. Surg., 1889, ix. 35 and 115. 

V olff, Oscar: “Die Caries der Synchondrosis sacro-iliaca und ihre Behand- 
lung.” Deutsche. Ztschr. f. Chir., 1898, xlix, 585. 

Zesas, Denis G.: “ Ueber die Tuberkulose des Iliosakralgelenkes.” Ztschr. 
f. Orthop. Chir., 1906, xv. 330. 


CHAPTER IX 


TUBERCULOSIS OF THE FINGERS AND TOES 


Tuberculosis of the bones and joints of tiie fingers 
and toes tuberculous dactylitis—of ten possesses some fea- 
tuies that distinguish it from the disease as ordinarily 
observed elsewhere in the skeleton. In adults it may 
oecui as an ordinary arthritis, like a tuberculous arthritis 
anyw here. In children it is seen as a tuberculous myelitis 
of the shafts of the metacarpals, metatarsals or phalanges. 
This is the so-called “spina ventosa,” 

Tuberculous Arthritis is rather a rare affection. 
I do not remember to have seen more than two or three 
cases in many years of clinical work, and have but two 


laboratory specimens. One of them, an amputated finger 
of an adult, shows far advanced synovial disease, with sec¬ 
ondary infection, and extension of the process to the bone 
marrow. Apparently it was a primary synovial case. The 
synovial membrane hangs in long streamers like moss from 


a tree. The patient died from pulmonary tuberculosis 
shortly after the operation. 

Another specimen represents tuberculosis of the meta- 
tarso-phalangeal articulation of the great toe, also in an 
adult. Its origin is impossible to determine, though 
the bone is badly involved. The treatment in this case 
was excision and it was followed by a cure. 

The structure of the hones entering into the articula¬ 
tions of the fingers and toes of an adult is that of the long 
hones generally, namely, cancellous bone at their ends, 

and dense bone with a medullary canal in the shafts. The 

22 


337 



338 


INFLAMMATION IN 150NES AND JOINTS 


$ * 



Fig. 110.—Tuberculosis of the metatarso-phalangeal joint. 

disease has no tendency to spread from one joint through 
the fatty marrow of the shaft to another. This fact is 
another link in the chain of evidence in behalf of the theory 
of the relation of the lymphoid marrow to tuberculosis. 


TUBERCULOSIS OF THE FINGERS AND TOES 339 


The symptoms are pain, swelling, sensitiveness, limita¬ 
tion of motion, etc. The diagnosis as a rule presents no 
peculiar difficulties, and is made on the points hitherto 
detailed. When the disease occurs in the metatarso¬ 
phalangeal joint of the great toe (I have never heard of 
a case in the other toes), it might be mistaken for gout. 
In gout there are almost always other evidences of the same 
disease elsewhere in the body, chalky deposits are present 
about the joint, and the Rontgen rays show the punched 
out areas in the bone near the joint. 

Treatment.— Conservative measures are hardly to be 
advised. A finger is of little importance. In the great toe 
the joint may be excised at the earliest possible moment, 
with the hope of saving a member that is of considerable 
importance in locomotion. The same treatment may be 
applied to a finger, but a stiff, deformed finger is not of 
much service, and most of us personally would probably 
prefer an amputation. 

Spina Ventosa. —Tuberculosis of the marrow of the 
shaft of the bones of the fingers, much more rarely of the 
toes, is fairly frequent in childhood, and in its essentials 
appears to be the same as tuberculosis of the shafts of the 
long hones of the extremities, a great rarity in this country, 
but evidently quite common abroad. The disease has prac¬ 
tically no tendency to attack the joints. Here we see a 
startling evidence of the truth of the statement that all 
definite infectious processes in bone, are alike in their 
fundamentals, and only differ in their details. We are 
reminded of suppurative osteomyelitis, which, when it 
involves the joints, has little tendency to spread to the 
shafts, and vice versa . 

The tuberculous process in the marrow of the shaft, is 
prone to break down early, become secondarily infected. 




340 


INFLAMMATION IN BONES AND JOINTS 


and establish a communication with the outside, resulting 
in the formation of a sinus which is difficult to heal. Some 
authorities affirm that the disease sometimes heals without 
breaking down, and without sinus formation, 1 but I do not 
remember ever to have seen such a case. 

New bone is said to be laid down in the periosteum, and 
through the hole in the cortex a probe can be passed into 
the diseased, apparently enlarged marrow canal. Some 
writers, basing their opinion upon radiographic evidence, 
deny the existence of new periosteal bone. Whether or not 
they are correct, the phalanx takes on a peculiar, enlarged, 
flask-like distended appearance (whence the name). 

Several phalanges may be affected, though not in the 
same finger, and this multiplicity of*the lesions distin¬ 
guishes the disease from tuberculosis in bone as ordinarily 
observed, and has given rise in some of the cases to a strong 
suspicion of syphilis, a suspicion strengthened by the bone 
production in the periosteum. 

Differential Diagnosis.— To distinguish tuberculous 
from syphilitic dactylitis is often an extremely difficult 
matter. The differentiation is to be made on the general 
principles heretofore set forth. 

Treatment. —Conservative treatment will usually be 
found preferable to radical. Sterile dressings, cleanli¬ 
ness, heliotherapy, passive hypersemia with Klapp’s suction 
cups, will be found useful. Some authorities recommend 
radical measures. The diseased bone may be dissected out 
subperiosteally and primary union of the wound can be 
secured, but in my experience little is gained in this way. 
As soon as the bone re-forms, the wound breaks down, and 
the trouble starts up as bad as ever. Some surgeons have 

1 Tillmanns: “ Lehrbuch der allgemeinen Chirgurgie.” Leipzig. Robert 
Veit 11. Co., 1892. 





TUBERCULOSIS OF THE FINGERS AND TOES 341 


reported success with bone transplanted from the tibia, or 
from a toe. 

Tuberculosis of the ribs is of fairly frequent occur¬ 
rence. It is manifest ordinarily by a comparatively pain¬ 
less swelling, usually fluctuating, near the junction of the 
rib with its cartilage. It may be treated by aspiration 
and injection, heliotherapy, etc., but usually resection of 
a portion of the rib will be necessary. 

Tuberculosis of the sternoclavicular articulation, of the 
pelvic bones, of the scapula, etc., are more or less curiosities. 
They are diagnosed and treated on the principles already 
laid down. The same may be said of tuberculosis of the 
bones of the bead and face, except that the disease is fairly 
frequent in some of them, such, for instance, as the mastoid 
process of the temporal. 

REFERENCES 

TUBERCULOSIS OF THE FINGERS AND TOES 

Aherns: “Demonstration von freien Knochentransplantationen." Berl. klin. 
Wchnschr., 1909, xlvi. 2167. 

Ehrhardt, O.: “ Ueber die Mulhersche Operation bei Spina ventosa.” Munch, 
med. Wchnoclir., 1903, i, 1665. 

Gaston et Gineno: “ Tuberculose papillomateuse du doigt chez un cordonnier 
bronchitique andien et a repetition, atteint de micro-polyadenopathies." 
Bull. Soc. Franc, de Dermat. et Syph., 1905, xvi, 52. 

Green, R. M.: “Tuberculous osteomyelitis of the digits.” Bost. Med. Surg., 
Jour., 1913, clxviii, 797. 

Veluet, Maurice: “ L’aspect Radiographique des Spinas Ventosas.” Theses 
de Paris, 1908-1909, xxxvii. 












. 








. 

: ' ■ " - ' 

* 




. 































SECTION VI 


OTHER FORMS OF ARTHRITIS OF THE 
FIRST GREAT TYPE OR GROUP 




























CHAPTER I 


COCCIDIOIDAL GRANULOMA 

To possess a knowledge of the pathology and symp¬ 
tomatology of tuberculosis is to possess a knowledge of 
the pathology and symptomatology of all the members of 
the group of which it is so conspicuous an example. Their 
fundamental characteristics are the same, and, while each 
possesses individual peculiarities which identify it with 
reasonable certainty in the great majority of cases, in no 
instance is the identification complete without the demon¬ 
stration of the causal organism. In some of them, as, for 
instance, tuberculosis and coccidioidal granuloma, this 
demonstration can be made, in others it is often impossible, 
and the cases recover, or progress for years, under a diag¬ 
nosis that must never be regarded as anything more than 
presumptive. The aetiology of some of them is 
known; the aetiology of others has almost been estab¬ 
lished; the aetiology of others is absolutely unknown. 
To take refuge in such terms as “faulty metabolism,” 
“diatheses,” or “rheumatoid” will not help us. 

In dealing with cases in this great group, one interest¬ 
ing fact is always to be borne in mind: They all look alike, 
and the clinical diagnosis is never made from an examina¬ 
tion of the joint itself, but from the history and from an 
examination of the entire patient. 

The members of the group which chiefly interest us are: 

1. Syphilitic and tuberculous arthritis. These have 
already been considered. The diagnosis of tuberculosis 
can be made positively. That of syphilis is usually 
presumptive. 


345 


346 


INFLAMMATION IN BONES AND JOINTS 


2. Coccidioidal Granuloma. In this a positive diag¬ 
nosis is possible. 

3. Chronic arthritis due to the diplostreptococcus. 
The causal organism has been demonstrated in some of the 
suspected cases, in others it has not. With improved tech¬ 
nique, the demonstrations have become more frequent. 
The domicile of the organism is presumed to be, in the 
great majority of cases, the tonsil or the deep urethra, 
but positive proof is lacking. A chronic osteomyelitis at 
the roots of the teeth is also thought by most observers to 
be a possible primary focus, but I believe that this 
lesion causes an entirely different type of disease, and is 
never the cause of this type of chronic arthritis. 1 

4. Chronic, progressive, multiple arthritis, which dif¬ 
fers from the preceding in its steady and remorseless pro¬ 
gression, its production of fibrous ankylosis in almost 
every joint in the body, its crippling flexion deformities, 
and in the fact that its cause is absolutely unknown. 

5. Still’s Disease, the multiarticular form as it occurs 
in children. 


COCCIDIOIDAL GRANULOMA 

The oidium coccidioides is a yeast fungus, in this coun¬ 
try almost exclusively domiciled in the San Joaquin valley 
in California. Practically all the patients afflicted with 
the disease which it causes, have lived at some time in or 
about the town of Los Banos. It produces in the bone 
marrow an inflammation whose symptomatology and clini¬ 
cal course are identical, up to a certain point, with those of 
tuberculosis. The effect of this inflammation upon the 
bone and upon the joint tissues is also the same as is that 

1 Ely, Leonard W.: “The great second type of chronic arthritis.” Archives 
of Surf/., 1920, i, 158. 



COCCIDIOIDAL GRANULOMA 


317 


of a tuberculous inflammation, so that the Rontgen picture 
of the one cannot he distinguished from that of the other. 
The likeness of the two diseases is so great that even the 
California surgeon usually mistakes the rarer affection for 
the more frequent, and only becomes aware of his mistake 
when the bacteriologist informs him of the presence in a 
cold abscess of the characteristic spores. 

“The parasitic organisms which cause the disease are 
easily found in the tissues, in the pus and in the sputum. 
They appear as spherical bodies about 30 microns in diam¬ 
eter with double-contoured capsules and a slightly granular 
protoplasm which is sometimes vacuolated. The capsule 
is highly retractile, and in some cases seems to have short 
knobs or prickles on the outer surface. A true nucleus has 
never been demonstrated. In the tissues these spherical 
bodies are found in the diseased areas in large numbers, 
usually within the tubercles, and frequently inside the 
multinuclear giant cells. In the walls of the abscess cav¬ 
ities and in the pus they are usually very numerous, and 
can be demonstrated with little difficulty. In the pus or 
in the sputum they are best seen in a fresh specimen pre¬ 
pared by placing a cover-slip over a drop of the material 
on a glass slide. If examination is made with but little 
light, the spherules stand out prominently and are easily 
distinguished from cells and from the myelin droplets 
which are also usually present. The bodies stain poorly 
with the ordinary staining methods and are very apt to 
be overlooked in the stained smear. 

“Reproduction within the tissues occurs by a process 

of endosporulation, and the organism differs from the 

blastomvces in that true budding has never been observed. 
%/ 

The spores develop by a division of the protoplasm within 
the capsule until a large number, a hundred or more, are 


348 


INFLAMMATION IN BONES AND JOINTS 


formed, and when mature, they are so closely packed 
together that they assume various shapes. They are re¬ 
leased through a rupture in the capsule of the parent body, 
and it is not at all uncommon to find a number of the empty 
envelopes in a specimen of pus. The development of the 
adult forms from the spores has not been definitely traced, 
because the spores are so small and they stain so poorly 
that it is impossible to follow the changes that occur after 
they escape from the parent body. However, Ophuls was 
able to find a few cases in which spores seemed to mature 
within the body of the parent before rupture of the capsule 
liberated them, and he believes that the adult forms develop 
directly from the spores by simple growth, without further 
change than the formation of the relatively thick, double- 
contoured capsule.” 2 

There are a few slight differences in the clinical behav¬ 
ior of coccidioidal granuloma and tuberculosis which, if 
the surgeon be on his guard, may possibly help him to 
distinguish the two. The former is perhaps not quite so 
prone to be confined to the ends of the long bones, nor 
to correspond to the distribution of the lymphoid marrow. 
The lesions are more likely to be multiple, and involvement 
of the viscera is frequent. The pain, muscular spasm, and 
deformity are perhaps not so great, in proportion to the 
damage to the bone as revealed by the X-rays. 

Treatment is usually of no avail. All the reported 
cases, except one, terminated fatally, and this is said to 
have recovered under the administration of iodide of 
potassium. The cold abscesses should be aspirated under 
strict asepsis, and every effort should be made to prevent 
the establishment of a communication between the focus of 
the disease and the outside air. 

2 Dicksox, Erxest C.: “ Oidiomycosis in California, with especial reference 
to coccidioidal granuloma” Arch. Inter. Med., 1915, xvi, 1028. 





CHAPTER II 

CHRONIC DIPLOSTREPTOCOCCIC ARTHRITIS 

^Etiology. —Upon considerable evidence, elinical and 
experimental, the diplostreptococcus domiciled in the ton¬ 
sil, deep urethra, and occasionally also in other organs, is 
assumed to be the cause of a form of chronic arthritis, 
whose clinical manifestations vary, but whose pathology 
and symptomatology are fairly well defined. This is the 
“infectious” arthritis of Goldthwait, and part of the “pro¬ 
liferative form” of Nichols and Richardson, and of the 
“rheumatoid” arthritis of the English. 

Sometimes the fluid and joint tissues are sterile, some¬ 
times they yield a diplococcus, sometimes a streptococcus 
“rheumaticus,” sive “viridans,” sive “hsemolyticus.” Pure 
cultures of these organisms often produce in laboratory 
animals a similar form of arthritis, and from the affected 
joints of these animals the organisms can be recovered. 
Rosenow is authority for the interesting statement that all 
these organisms are really one and the same, simply chang¬ 
ing their form according to the conditions under which 
they find themselves. They can be recovered from the 
mouth of normal individuals, and in ordinary circumstances 
are harmless, but when growing under pressure, as, for 
instance in the deep crypts of the tonsil, or in the seminal 
vesicles they may take on £>athogenic properties. When 
growing in the tonsil, their virulence is affected by changes 
in the secretion of the mouth; hence the well recognized 
influence of the emotions and of digestion in the aetiology 
of the disease. Chilling of the surface of the body, per¬ 
haps by lowering the resistance, seems to be a pre¬ 
disposing factor. 


349 


350 INFLAMMATION IN BONES AND JOINTS 

When the focus is in the deep urethra, this form is 
often called chronic gonorrheal, or chronic gonococcic 
arthritis, but it is doubtful if the gonococcus, even if pres¬ 
ent, is ever responsible for these old, chronic arthritides. 
The cause is probably the other organism, grafted upon 
the original infection. In other words we have here again 
a case of secondary infection. The gonococcus causes an 
acute arthritis, and its presence in the joint is fleeting. 
It does its work quickly, and disappears. 

We find, therefore, in patients with this type of arthri¬ 
tis’ evidences of chronic tonsillitis, of chronic prostatitis, 
of seminal vesiculitis, etc. The suspicious tonsil is as a 
rule not the large, succulent, hypertrophied one as might 
be thought, but the small, fibrous, buried one. Sometimes 
the j)atient will give a history of frequent attacks of sore 
throat; perhaps more often he will give a history of having 
had attacks many years previously, even of attacks of 
quinsy, but without further throat trouble in years. 

Chronic infection of other organs, such as the gall blad¬ 
der and the female genitals, has also been held responsible 
for this form of arthritis. This may be true, but I am 
somewhat sceptical of it. 

Pathology. —We have not the same abundance of 
pathological material of cases of this disease as we have of 
tuberculosis, and our knowledge of the pathology therefore 
is not so nearly complete, but from what we do possess 
it appears that the essentials of the pathology of the two 
diseases are much the same. There is the same prolifera¬ 
tive inflammation in the marrow, and in the synovial mem¬ 
brane, with a similar effect upon the bone and cartilage, 
but, apparently, in the majority of cases, in contradistinc¬ 
tion to tuberculosis, the burden of the attack is borne by 
the synovial membrane rather than by the marrow. The 


CHRONIC DIPLOSTREPTOCOCCIC ARTHRITIS 351 

bone in the vicinity ot the joint is absorbed to a greater or 
less degree, and probably the cartilage is attacked from 
beneath by the granulation tissue in the marrow, and per¬ 
forated. Adhesions form between the marrow and the 
synovial membrane, and between the marrow of one hone 
and the marrow of the other. 

A hyperplastic inflammation may take place in the 
synovial membrane, with an abundant villous formation. 
This is the so-called villous arthritis of some writers. In 
such a case a fluid is poured out into the joint, usually 
serous in its nature. On the other hand this reduplication 
of the synovial membrane and villous formation, may be 
absent, as in tuberculosis, and fibrous changes may pre¬ 
dominate. In such case the joint will be dry, and shrunken 
rather than swollen. Naturally in the latter case, the ad¬ 
hesions in the joint would be much more in evidence than 
in the former. 

The disease shows a marked predilection for certain 
joints. The spine may be affected in whole or in part. 
A localized involvement, as occurs in tuberculosis, is, at 
best, very rare. The typical lesion is an arthritis of all 
the spinal joints except the two uppermost. The hips and 
shoulders usually escape, the wrists, knees, ankles, and 
tarsus are frequently involved. A multiple arthritis of 
the finger joints is characteristic of some cases, especially 
of those caused by disease in the tonsil. Strangely enough, 
and in contradistinction to the second great type of arthri¬ 
tis, the metacarpophalangeal, and the proximal interphal- 
angeal joints are attacked, while the distal interphalangeal 
joints escape. Temporo-mandibular arthritis is fairly 
frequent. 

Secondary infection and suppuration are extremely 


352 


INFLAMMATION IN BONES AND JOINTS 


rare, if they ever occur. I do not remember ever to have 
seen abscess formation in one of these cases. 

The duration of the disease varies. It may be fleeting, 
it may persist indefinitely, or it may clear up at any time, 
following treatment. It may disappear and recur, espe¬ 
cially if its cause have not been removed. Complete recov¬ 
ery may follow an attack, or the fibrous adhesions may 
cause an ankylosis more or less complete, according to 
their amount and density. This fibrous ankylosis may be 
permanent, or with time it may slowly yield and allow a 
fair degree of motion, especially if the original cause have 
been removed. In the last analysis the degree of perma¬ 
nent ankylosis seems to depend upon the amount of dam¬ 
age to the joint cartilage. 

Course.— One joint alone may he affected, but if the 
disease last any length of time, practically invariably it 
shows a multiarticular tendency. This may be said to be 
characteristic of it. Sometimes only two or three joints 
are involved, at intervals, or all together. If many joints 
are involved, more or less of a tendencv to svmmetrv is 
wont to be present, especially in the case of the hands and 
feet. The inflammation does not disappear from one joint 
as the next one is attacked, as it does in acute inflammatory 
rheumatism, but persists. The progression may be more 
or less steady, or it may be characterized by remissions. 

Symptomatology. —The symptoms and physical signs 
are those common to all the members of this type of arthri¬ 
tis, namely, pain, usually swelling, sensitiveness to pres¬ 
sure, disability, limitation of motion, and muscular atrophy. 

The pain varies. It may amount to no more than a 
feeling of slight discomfort and stiffness, or it may be very 
severe. Roughly, one might say that it about equals the 
pain of an ordinary case of synovial tuberculosis, but rarely 



CHRONIC DIPLOSTREPTOCOCCIC ARTHRITIS 353 

equals that of joint tuberculosis with bone involvement. 
I lie pain is rather severe in the acute exacerbations, but 
not so great during the remissions of the disease. It is 
worse, of course, on motion. 

If swelling be present, it is as a rule due to fluid in the 
joint rather than to thickening of the synovial membrane, 
though especially in the fingers, the soft parts may be 
decidedly thickened. The synovial membrane is almost 
invariably sensitive to pressure. When the disease is in the 
lower extremity, the patient limps. The limitation of mo¬ 
tion ranges from a slight limitation at extremes, to an 
almost complete absence of motion. It is usually marked, 
and is due to the fluid in the joint, to the thickened synovial 
membrane, to the adhesions, both in the joint, and in the 
neighboring tendon sheaths, and to the muscular spasm. 
Muscular spasm, and muscular atrophy may be prominent, 
but not as prominent as in tuberculosis. 

Diagnosis. —The pain, swelling and limitation of mo¬ 
tion make the diagnosis of an arthritis a simple matter. 
The next step is to ascertain in which type of arthritis the 
case belongs. This is done on the symptoms, and chiefly 
on the X-ray evidence. An arthritis of the second great 
type shows a lower grade of inflammation, as a rule less 
pain and a range of motion that is practically painless, 
and is only limited at extremes, and then only by the me¬ 
chanical obstruction of the new bone formation. The 
X- ray plate shows the new bone formation at the line of 
insertion of the capsule, with spurring and lipping, in the 
second type. 

Having ascertained the type, we next try to establish 
the identity of the particular member of the type. The 
other members which most merit consideration, are tuber- 


23 


354 


INFLAMMATION IN BONES AND JOINTS 


culosis, syphilis, and the hopeless progressive form later 
to be described. 

Tuberculosis is to be suspected in a slow, chronic, pain¬ 
ful inflammation in a single joint, more or less steadily 
progressing, and with no appreciable tendency to recovery 
without treatment. The muscular spasm and the mus¬ 
cular atrophy, probably on account of the more extensive 
disease in the bone, are greater than in the form of arthritis 
under consideration. The history may help us, and the 
physical examination of the patient himself, but we must 
not permit ourselves to be too much swayed by their result. 
A patient with pulmonary tuberculosis may have a diplo- 
streptococcus arthritis, and a patient who gives a history of 
many Neisserian infections and frequent sore throats, may 
have a tuberculous joint. The only sure test is by the 
demonstration of the causal organism. This may be im¬ 
possible in a diplostreptococcic inflammation, but it is 
almost invariably possible in a tuberculous joint. 

Syphilitic joints rarely show the same amount of fibrous 
adhesions as this form, but personally I know no way to 
differentiate the two except by the therapeutic test. The 
history, the glandular enlargement, the Wassermann and 
Noguchi tests are all suggestive but not conclusive. Of 
course, if the patient give a distinct history of syphilis, and 
show definite stigmata of the disease, the presumption of 
a syphilitic arthritis is justified. 

The fourth member of the type is recognized by its 
steady, remorseless progression in spite of all treatment, 
by its stiff, shrunken joints, and its contractures. In their 
early stages the two forms cannot be distinguished. It is 
only the absolute failure of the one to respond to treatment, 
and its slow, steady progression, which enable us to dis¬ 
tinguish it from the other. 


CHRONIC DIPLOSTREPTOCOCCIC ARTHRITIS 355 

Gout also may be considered in this connection. True 
gout is rare in this country, at least in the three widely 
separated parts of the country in which I have lived. It 
has a marked predilection for the metatarsophalangeal 
joint of the great toe, and the characteristic chalky deposits 
in the cartilages of the ear and the joints. The X-ray 
plate shows the punched out areas near the joint line. 

The arthritis of gout is probably a traumatic arthritis 
caused by the deposition in the joint cartilage of crystals 
of biurate of soda. Its treatment is essentially within the 
domain of internal medicine, though the attacks of acute 
arthritis may perhaps be rendered less painful by rest. 

Prognosis. —The prognosis is on the whole good. In 
the early stages, however, on account of the difficulty or 
rather the impossibility of distinguishing this form from 
the hopeless progressive form, in the early stages, the prog¬ 
nosis must be guarded. Any multiple, progressive arthri¬ 
tis must be viewed with suspicion until its nature is known. 
As has been said, the bone and cartilage changes in this 
form usually are not great, and, as long as the disease is 
confined to the synovial membrane, there is no reason why 
complete recovery should not take place. 

TREATMENT 

This consists first and foremost in the removal of the 
cause. If the tonsils are suspected, they should be excised 
in toto. If no other focus be discovered, the tonsils, even 
if they appear normal, should be removed. If any evi¬ 
dences of infection be found in the deep urethra, treatment 
should be directed to that region. Sometimes irrigations 
and dilation, and prostatic massage will accomplish the 
purpose; often seminal vesiculotomy will be necessary. 
Tonsillectomy often is not followed by immediate improve- 


356 INFLAMMATION IN BONES AND JOINTS 

merit. Indeed the operation is sometimes followed by an 
aggravation of the symptoms, and this aggravation is 
rather a favorable portent. A period of rest will be of 
advantage after the operation, in the severe cases even a 
week or two in bed. 

After the removal of the focus, the joint, or joints, 
may return to normal, or to a condition approaching nor¬ 
mal. If the symptoms continue, there are various meas¬ 
ures which promise more or less relief. Chief among these 
perhaps is the deep intramuscular injection of a foreign 
proteid. The identity of the proteid is probably a matter 
of indifference. Antigonococcic serum or vaccine, ty¬ 
phoid vaccine, or horse serum may be tried. Baking, 
hydrotherapy, heliotherapy, and gentle massage have their 
advocates. Their rationale does not seem quite clear, but 
they may do good, nevertheless. If the pain be severe, 
immobilization may still it, but immobilization in this form 
of arthritis rarely is of much permanent benefit. 



CHAPTER III 


CHRONIC PROGRESSIVE MULTIPLE ARTHRITIS 

This form differs from the preceding, as has been said, 
chiefly in its more or less steady progression, in its utter 
lack of response to 
treatment, and in the 
fact that nothing is 
known as to its cause. 

It is seen most fre¬ 
quently in young or 
middle aged women. 

The essentials of its 
pathology are the 
same as those of the 
preceding form. 

The disease usu¬ 
ally begins insidi¬ 
ously with pain and 
swelling in one or 
more joints. The 
joint stiffens. Then, 
one after another, the 
other joints become 
involved, until the 
patient becomes a 
hopeless, bed-ridden cripple. While there is no absolute 
rule of progression, the disease manifests a distinct ten¬ 
dency to symmetrical distribution. The acute symptoms, 
having lasted for awhile in a joint, may subside, leaving 

357 


Fig. 111. —Vow power photomicrograph of the bone at 
the articular surface, from a case of chronic arthritis 
of the first great type—the so-called rheumatoid arthritis. 
The specimen was removed at necropsy. Only the mul¬ 
tiple lesions and the absence of tubercles in the marrow 
distinguish it from tuberculosis. 



358 


INFLAMMATION IN BONES AND JOINTS 


the joint more or less distorted and crippled. The joint 
thereafter is subject to other attacks, each one of which 
leaves it in worse condition. For weeks, perhaps, these 
attacks may be absent, and the patient and her friends 
think that she is on the mend; then the attacks recur. 

The joints become ankylosed in semiflexion. The 
deformity is hard to prevent, and difficult to overcome 
when it has taken place. The wrists are in ulnar deviation. 
In America, indeed, this disease is often alluded to as 
“arthritis deformans,” though it is quite distinct clinically 
and pathologically from the original arthritis deformans 
as described by the Germans. It is also sometimes called 
rheumatoid arthritis. 

This form of arthritis has no set duration. For a 
long time, in the intermissions, the patients may be fairly 
comfortable, and their general condition may be fairly 
good. Sooner or later, some intercurrent disease, such as 
pneumonia, closes the scene. Sometimes a nephritis 
supervenes, and this fact justifies a supposition that an 
obscure infection is at the root of the trouble. 

The prognosis is hopeless. I have been called to see 
a patient in the earliest stage of the disease, before there 
was any objective sign of an arthritis, except the merest 
suspicion of stiffness in the spine. I have watched her 
grow worse in spite of everything I could do, and I have 
seen her later as a clinic patient in the University hospital 
with all the resources of the staff at her service. Nothing 
that anyone could do was of any avail to check the onward 
march of the disease. 

The Treatment is symptomatic. The coal tar deriv¬ 
atives may check the pain, perhaps, in addition to external 
applications. Heat or cold may give relief. During the 
acute attacks splinting may be advisable. Morphine, on 


359 


PROGRESSIVE MULTIPLE ARTHRITIS 

account of its unfortunate after effects, must be employed 
sparingly, but sooner or later will probably be found neces- 
sa i> • Diet has no permanent effect upon the disease, 
and absolutely none in causing it, but of course the food 
should be carefully chosen and should be easily digestible. 
Fresh air and sunshine help to keep the patient in good 
general condition. „ Antisyphilitic treatment will always 
be tried and will invariably be found of no avail. 


CHAPTER IV 


STILL’S DISEASE 

CHRONIC POLYARTHRITIS IN CHILDREN 

In 1897 Still 1 first drew attention to a form of polyar¬ 
thritis in children, and published twelve cases of the disease. 
Since then several other observers have added reports of 
cases, but without clearing up the a 3 tiology or the path- 
ologv. Evidently Still s disease belongs either in the third 
or fourth division of this great type of arthritis. Formerly 
it would have been classed distinctly in tbe fourth division, 
on account of its fatal termination, but the improvement, 
or recovery of several cases, and at least a rational guess 
as to the etiology indicate that eventually it will be placed 
in the third, or at least, that many of the cases of it 
will be. 

./Etiology.— Nothing definite is known as to this, but 
the \\ hole picture is that of a chronic infection. Reasoning 
from analogy we suspect the tonsil rather than the teeth. 

1 aihologv . I ha\ e not been able to find any account 
of an examination of the bone marrow, but the findings of 
se^eial observers reveal that the changes in the synovial 
membrane and cartilage are typical of this type of arthritis; 
namely, the synovial proliferation, with the encroachment 
on the cartilage at its periphery, and the thinning and per¬ 
foration of the cartilage. Rarefaction of the bone is shown 
by the X-ray, and in Whitman’s case an enlargement of 
the proximal ends of the second row of metacarpals which 
might be mistaken for a spina vento sa. The skiagrams 

Still, G. T.: “On a form of chronic joint disease in children.” Medico- 
Chirurgical Society Transactions, London, 1897, lxxx, 47. 

360 






STILL’S DISEASE 


361 


of several joints in Rosenf eld’s case might be mistaken for 
tuberculosis in the absence ot a history. Neither lipping 
nor spurring is present. 

Hyperplasia of the lymph nodes, more or less general, 
is invariable. In one or two cases the mesenteric lymph 
nodes showed amyloid degeneration. The spleen is always 
enlarged, the liver often enlarged, and both may show 
amyloid degeneration. The same is true of the kidneys. 
Pericardial and pleural lesions are frequent, with or with¬ 
out valvular change. The thyroid may be enlarged, and 
exophthalmos may be present. 

Symptomatology. —Still’s disease usually begins with 
chills, fever and sweating. At the onset, or some time 
afterward, the joint symptoms appear, with swelling, lim¬ 
itation of motion and pain. The larger joints are usually 
affected first, especially the knees, then, in much the same 
manner as in the preceding division, the other joints of 
the body become involved, one after the other, and more 
or less symmetrically, and as a rule to the accompaniment 
of constitutional disturbance. The sternoclavicular joint 
usually escapes. The same flexion deformities, contrac¬ 
tures and swelling are observed as in the proceeding class, 
even to the ulnar deviation of the hands. In contradistinc¬ 
tion to the second great type of arthritis, the fingers in 
this disease, as in the other members of the type, show 
involvement of the proximal interphalangeal, rather than 
of the terminal joints. 

The disease has its periods of acute exacerbation. In 
the intervals of the attacks, the patient may he fairly 
comfortable. 

Various skin eruptions have been noted, and blood 
changes are characteristic; namely, leucocytosis, eosino- 
philia, and, sometimes, degeneration in the red cells. 



362 


INFLAMMATION IN BONES AND JOINTS 

These indicate extensive marrow disease. The lymph 
nodes are palpably enlarged, and usually increase in size 
during the acute exacerbations. The characteristic en¬ 
largement of the spleen can be made out, and often the 
enlargement of the liver. 

Ihe thyroid gland may be enlarged, and exophthal¬ 
mos may be present. The urine often contains albumin. 

Muscular atrophy is extreme and the shrinking of 
the muscles exaggerates the appearance of swelling in 
the joints. 

Prognosis. —The early cases reported all ended fatally. 
Recoveries have been reported in later cases, some of them, 
strangely enough, after an intercurrent infectious disease 
•—scarlatina especially. 

Treatment. —The first indication is to find the cause, 
if possible, and to remove it. The tonsils come first. 
They should be excised, and any other focus should be 
cleaned up. Even the middle ear and the sinuses should 
not be o\ erlooked, if no improvement follow tonsillectomy. 
One patient showed improvement after the injection of a 
foreign protein. Palliative treatment may be advisable 
for the pain—splinting, heat, salicylates, etc. In the inter¬ 
vals, massage may be of benefit. 



SECTION VII 


THE SECOND GREAT TYPE OF CHRONIC 

ARTHRITIS 







CHAPTER I. 

THE SECOND GREAT TYPE OF CHRONIC ARTHRITIS 

Synonyms: Hypertrophic Arthritis, Degenerative 
Arthritis, Osteoarthritis, Arthritis Deformans, Metabolic 
Arthritis, Senile Arthritis. 

iETIOLOGY 

This is the mysterious type of arthritis, whose exact 
aetiology always has been in doubt. It is an ancient disease, 
as evidenced by its characteristic marks on bones of a 
great age. While its prevalence is greater in some regions 
than in others, its distribution is very wide, perhaps univer¬ 
sal. It is essentially a disease of middle and of later life, 
and it never occurs in childhood. The term “arthritis 
deformans juvenilis” is a misnomer. I think that no case 
in a child ever has been published, which showed the lesions 
characteristic of the disease. The exact time of its inci¬ 
dence is sometimes hard to determine, but in 90 cases 
tabulated at the Stanford Clinics, the patients, when they 
presented themselves for treatment, were in the third 
decade of life in 2 cases, in the fourth in 12 cases, in the 
fifth in 26 cases, in the sixth in 32 cases, in the seventh 
in 15 cases, in the eighth in 3 cases. Almost two thirds of 
the patients were between 40 and 60 years of age. As the 
symptoms dated back some time before the patients were 
seen, it is evident that the onset of the disease is earlier 
than these statistics show. The age of the youngest pa¬ 
tient was 28 years, of the oldest 60. 

Various views have been advanced as to the prime 
cause. Most writers recognize a traumatic element in the 
causation, and some consider trauma the sole cause. 

365 


366 


INFLAMMATION IN BONES AND JOINTS 



Fra. 112.—Distal end of two femora showing the typical lipping of the great second type of chronic arthritis. 







SECOND TYPE OF CHRONIC ARTHRITIS 


367 


Axhausen, as the result of laboratory experiment, main¬ 
tained that the disease regularly followed injury to the 
articular cartilage. 1 Ely and Cowan reached conclusions 
diametrically opposite. 2 Chronic strain, whether due to 
laborious occupation, or to deformity elsewhere in the body, 
has been linked up in a causal relation, but the disease 
occurs in people in all ranks of life, and in the young it 
never follows dislocations, rotary lateral curvature, or even 
bow-legs and knock-knees. 3 

Many writers regard infection as the cause of the dis¬ 
ease, but I have never been able to find reliable evidence 
of infection in any case. The evidence on this point was 
purely presumptive. Believing firmly that the infection 
was there, I have made unremitting but until recently vain 
efforts to find it. We must not permit our enthusiasm in 
these matters to influence our conclusions. 

Exposure to cold and dampness, chilling of the surface, 
emotional and digestive disturbance, have all been held 
responsible, and there seems little doubt that these factors 
do influence the march of the disease, and aggravate the 
symptoms, but none of them is necessary to the incidence 
of the disease, and none of them is held to be its prime cause. 

According to some, mysterious chemicals, floating in 
the blood, act directly on the bone and cartilage, and pro¬ 
duce in them the characteristic changes. The terms “dys- 
crasia” and “diathesis,” “rheumatic” or other, are employed 

1 Axhausen, Georg: “ Ueber einfache; aseptische Knochen-und Knorpel- 
necrose, Chondritis dissecans and Arthritis deformans.” Arch f. klin, Chir., 
1912, xcix, 519. 

2 Ely, Leonard W., and Cowan, John Francis: “Reaction of the tissues 
of the knee-joint of the rabbit to injury: Bone and Joint Studies 1.” Stanford 
University, Cal. Published by the University, 1916. 

3 Patek: “Static deformities as factors in the production of so-called 
hypertrophic arthritis.” J. orth. surg., 1921, iii, 324. 





368 


INFLAMMATION IN BONES AND JOINTS 


in this connection, and at present “faulty metabolism” is 
quite popular. Faulty metabolism, when analyzed, means 
simply, disease. 

If one will carefully examine one s patients with this 
form of arthritis, one will find that practically all have 



Fig. 113.—Photograph of a resected knee from a typical case of chronic arthritis 
second type. Tibia on the left, condyles of the femur on the right. 


of the great 


one thing in common, namely, evidences of a chronic 
osteomyelitis about the roots of the teeth. I have found 
it in every one of my private patients. Two only of all 
my clinical patients, in whose history the condition of the 
teeth w as noted, had sound teeth. The iX-rays showed 
extensive rarefaction in the bones. 

No direct proof of the causal relation of alveolar infec- 



SECOND TYPE OF CHRONIC ARTHRITIS 


369 


tion to the arthritis ever has been adduced, but the circum¬ 
stantial evidence that a causal relation exists, is almost 
overwhelming. This hypothesis would explain the well 
known predilection of the disease for later life, and in 
earlier life only when the teeth are affected. It would 
explain also the influence of emotional and digestive dis¬ 
turbance, possibly also that of wet and cold, through the 
change in the secretions of the mouth. As I shall attempt 
to show, the primary changes about the joints are in the 
marrow in the vicinity. The changes in the cartilage and 
bone are secondary to them. Trauma acts by spraining a 
joint already damaged and distorted by the disease. A 
damaged machine is easily injured. Trauma is the cause 
of the subjective symptoms, not of the disease itself. On 
the other hand, trauma is probably the cause of the arthritis 
itself, that is, of the inflammation in the synovial membrane. 

In my earlier work I considered the alveolar osteo- 
myelitis as the direct cause of the disease, but the two 
patients with sound teeth negatived this theory, as well 
as the inherent improbability of it. The most probable 
hypothesis is that the offending organism is domiciled in 
the intestinal tract, and is ordinarily harmless as far as the 
joints are concerned, unless it have a port of entry. The 
alveolar osteomyelitis furnishes this in the vast majority 
of cases. The organism may be a protozoon, and a group 
of us are working to find out its identity. The necrosis 
in the bone points to the amoeba histolytica as the culprit . 4 

4 Since the above was written we have found the amoeba in the bone 
marrow of one case, and have reason to believe that we shall find it in 
others. If the finding be confirmed, the subject will be put on a scientific 
basis. 

Ely. Leonard W., et al. : “ The amoeba as the cause of the second great 
type of chronic arthritis.” Cal State Med. Jour., 1922, xx, No. 2. 


24 





370 


INFLAMMATION IN BONES AND JOINTS 



Fig. 114. —Chronic arthritis of the great second type. Note spurring on the condyle and 
tuberosity, and the cavity at C. The presence of cavities in the bones was demonstrated 

at operation in this case. 

PATHOLOGY 

The gross pathological changes in this type of arthritis 
have had extensive mention, and are well known to many 
who are called on to treat bones and joints. Very few 



SECOND TYPE OF CHRONIC ARTHRITIS 371 

have attempted to work out the pathological histology 
Nichols and Richardson’s work is a classic in this line. 



Fig. 115.—Sections of head of femur from a case of second type arthritis. S, sequestrum. 

When one examines a specimen of this form of arthritis 
in the laboratory, three things are prominent in the naked 
eye inspection: 

1. Thickening, reduplication and villous proliferation 
in the synovial membrane. 

2. Partial or complete disappearance of the articular 
cartilages, with a dense, hard, polished, eburnated (ivory- 

~Nichols, E. H., and Richardson, T. L.: “Arthritis deformans.” Jour . 
Med. Research, 1909, xxi, 149. 















372 


INFLAMMATION IN BONES AND JOINTS 


like) condition of tlie subjacent bone. This bone is often 
grooved in the line of joint motion. 

3. Masses of bone and cartilage built up at the margin 
of the articular cartilage, at the line of attachment of the 
capsule. It is these masses of new bone which show in the 
X-ray plate, and enable one to recognize the disease clini¬ 
cally, and are responsible for most of the names that have 
been bestowed upon it. Pieces of bone and cartilage may 



Fig. 116.—Photograph of a stained slide from section A of the preceding. 

S—Sequestrum. L—Lipping. 

lie loose in the joints, or may be attached to the bone end 
or to the synovial membrane. 

LTpon sectioning the bone one finds larger and smaller 
places in which the bone tissue is lacking. 0 These spaces 
may be filled with fibrous marrow, or they may be the seat 
of cysts, large and small. Sometimes fibrous tissue and 
cysts are intermingled, the proportion of each varying in 
different sections. 7 Small pieces of dead bone may be 

6 Ely, Leonard W.: “A study of 100 dry bones sawn in the laboratory; 
Bone and Joint Studies 1.” Stanford University, Cal., published by the 
University, 1916. 

7 Ely, Leonard W.: “The great second type of chronic arthritis.” Arch . 
of Surg., 1920, i, 158 











SECOND TYPE OF CHRONIC ARTHRITIS 


373 


found in the fibrous tissue. Occasionally a large part of 
the end of the bone may be nothing but an aseptic sequest- 


C 



Fig. 117.—Photographs of stained slides from sections taken 
a short distance from each other from the head of the femur in 
a case of second type arthritis. Note cavities at C, the layer of 
dense bone, D, at the articular surface of the bone and the 
rather open meshed bone beneath it. 

rum. The aseptic necrosis is probably the primary 
morbid change. 

The ridges of bone at the margin of the joint cartilage, 
the lipping or border exostoses, as they are called, are seen 








374 


INFLAMMATION IN BONES AND JOINTS 


to consist of bone usually covered by cartilage, and raised 
above the level of the articular surface of the bone. New 
bone evidently has been laid down also in the marrow in 
the immediate neighborhood of the joint, for the bone 
tissue here is wont to be much denser than normal. Deeper 



Fig. 118.—Section through the neck of the femur from a case of 
second type arthritis. C, cavity. The cavity marked G, is an arti¬ 
fact caused by gouging out the bone for culture purposes. 

in, it is more open meshed than is normal bone in the 
same region. 

HISTOLOGY 

Besides all the bone patent to naked eye inspection, 
new bone can be seen forming in the marrow, both through 
the medium of cartilage and directly out of fibrous tissue. 
The marrow is mostlv fibrous and fattv. Here and there 
are areas in which all bone is lacking. Its place is taken 
by cysts and fibrous tissue in varying proportions. Some¬ 
times in the fibrous tissue small dead trabeculae can be dis- 












SECOND TYPE OF CHRONIC ARTHRITIS 375 

tinguished. I have one specimen of a femoral head, which 
consists of little else than a large sequestrum, but there 
is nothing in my specimens to indicate that arterial disease 
is the prime cause of the necrosis. Elsewhere the bone 
trabecuke are usually thicker and denser than normal. 

The joint cartilage is irregular both in its thickness and 
in its structure. In places it is thicker than normal, in 



places it may be absent altogether. Its structure is best 
described as bizarre. It sometimes presents a fantastic 
appearance. Generally it is fibriliated. Often its cells 
are swollen and distorted, often many of them have dis¬ 
appeared. Its surface may have a peculiar tattered look. 
Calcification of the cartilage to a greater or less extent 
is common. 

The marrow shows areas infiltrated by lymphocytes, 
and among the cells many plasma cells can be made out. 





376 


INFLAMMATION IN BONES AND JOINTS 

The synovial membrane is thickened and villous. The 
villi, while they may show some cellular proliferation at 
their surface, have not the cellular, “lymphoid” structure 
so common in the first type of arthritis, but consist usually 
of a loose-meshed reticulum of fibrous tissue containing* 
considerable fat. Bone and cartilage formation is said 
to take place in the villi. Lymphocytic infiltration takes 
place in the synovial membrane as well as in the marrow. 



. 120. Photograph of stained slide from a case of second type 
arthritis of the knee. Articular surface above. The arrows point 

to the necrotic areas in the bone. 


The absence of the cartilage, with the resulting expos¬ 
ure of the underlying bone, causes a grating and creaking 
of the joint when it is moved, and the fact has given rise 
to the opinion that the joint was “dry.” It is not dry, but 
usually contains an excess of serous fluid. 

In the spine, new bone formation takes place in the 
anterior common ligament, occasionally welding the verte¬ 
brae together. The usual production of bone consists of 
lipping of the vertebral bodies, as in other bones. In the 
other joints of the body union of the articulating bones, 

or by fibrous tissue, practically never 
takes place. The limitation of motion is caused by the 
roughening and distortion of the hone ends. The joint is 










SECOND TYPE OF CHRONIC ARTHRITIS 377 

damaged as a machine for locomotion. The cartilage, once 
worn off, never re-forms, and the new bone formation is 
never absorbed. 

When the disease occurs in the hip, it sometimes passes 
under the name of “morbus coxce senilis.” New bone is 
deposited not only about the femoral head and the acetabu¬ 
lum but also on the great trochanter. The head of the 



Fig. 121. —Eburnated bone at the articular surface in a case of second type arthritis. Low power 

photomicrograph. 


femur often becomes flattened, “mushroomed,” as it is 
called, and ceases to fit in the acetabulum. Actual dislo¬ 
cation however probably never takes place. The Rontgen 
film taken immediately after a fracture of the hip in the 
aged often shows the characteristic changes of this type of 
arthritis. The fracture does not cause the arthritis, nor 
does the arthritis cause the fracture, but both are caused 
by the same thing, namely, rarefaction in the head and neck 
of the femur. I think this rarefaction, but not necessarily 










378 


INFLAMMATION IN BONES AND JOINTS 


the arthritis, will always be found in the peculiar fracture 
of the femoral neck occurring in the aged. 

In the fingers, the disease affects by preference, the 
terminal interphalangeal joints, in contradistinction to the 
first type of arthritis, which affects usually the proximal 
interphalangeal and the metacarpophalangeal. The ter¬ 
minal phalanges become semiflexed, and slightly deflected 



Fig. 122.—Low power photomicrograph of articular cartilage 
from a case of second type arthritis. Note its bizarre appearance 
and the marked evidences of calcification. 


laterally. The bone jDroduction about the joint line gives 
rise to characteristic deformities, popularly known as 
Heberden’s nodes. These are sometimes considered as a 
manifestation of gout, but they have nothing whatever 
to do with that disease. Study of the X-ray pictures of 
these finger joints teaches us that the bone production is 
never as much as it appears clinically. Rarefaction and 
bone destruction dominate the picture. Unless this fact 
be borne in mind, one may err in the diagnosis. 




SECOND TYPE OF CHRONIC ARTHRITIS 


379 


This type of arthritis is practically always multiarticu- 
lar in its manifestations in the spine and in the fingers. 
When it occurs elsewhere, the symptoms may he confined 
to one joint, but if other joints be radiographed, the char¬ 
acteristic lesions will often be found in them also. The 
essential primary change, as we have seen, is probably in 
the marrow, and this change may exist for a long time, and 



Fig. 123. —Typical appearance of cartilage from a second type 
arthritis of the hip. Low power photomicrograph. Note calci¬ 
fication, fibrillation and “tattering.” 


may be widespread before it produces any symptoms in 
the joints. We regard the disease as an arthritis because 
it manifests its presence by joint symptoms, but funda¬ 
mentally it is perhaps the same process as that at the bot¬ 
tom of certain diseases of the shafts, described in another 
section.—Paget’s deforming osteomyelitis and osteomy¬ 
elitis fibrosa. 

Radiograjdis of intraarticular fractures in middle aged 
and elderly persons indicate that much of the stiffness 








380 INFLAMMATION IN BONES AND JOINTS 

following the fracture is due to the opening up of an old 
focus in the diseased marrow. Indeed it may well be that 
Colies’ fracture, for instance, as well as fracture of the 
neck of the femur, owes its frequency to a preexisting 
rarefaction in the bone. 



Fig. 124.—Rather high power photomicrograph of some of the 
cartilage tatters shown in figure 123. 


S Y M STOMATOLOGY 


The symptoms are those of a low grade chronic arthri¬ 
tis—pain, moderate swelling, stiffness, limitation of motion, 
disability, deformity, etc. 

The pain is rarely severe except in disease of the hip, 
and is almost always lessened by heat: Hence the tendency 
of elderly persons with “chronic rheumatism” to hug the 
fire. The joints, being mechanically damaged, are subject 
to strains and sprains. 1 hese are followed by an exacer¬ 
bation of the symptoms, and in the spine are called “neu¬ 
ritis, lumbago or sciatica. 4 he jiain is usually 









SECOND TYPE OF CHRONIC ARTHRITIS 381 

aggravated by cold and dampness. The joints of per¬ 
sons with this form of arthritis often constitute an 
excellent barometer. 

Errors of diet also increase the pain; lobster, straw¬ 
berries and tomatoes will often bring on an attack. 


Fig. 125. —Cellular infiltration in the marrow from a case of second type arthritis. Low power 

photomicrograph. 

Patients therefore think that they are “gouty.’ Any 
idiosyncrasy of diet may have its effect. Sometimes the 
pain is worse on rising, wearing away as the joint is used, 
but overuse increases it. The joint creaks and grates, 
sometimes audibly, almost always palpably. If the pain 
is severe, as in disease of the hip, or of the spine after strain, 
muscular spasm may be marked, otherwise it is not to be 










382 


INFLAMMATION IN BONES AND JOINTS 


expected. The spine may be held perfectly rigid during 
an acute attack. 


The swelling is usually moderate, and is due to the 
thickened synovial membrane, to the fluid in the joint, 



Fig. 126. —Low power photomicrograph of a section of the synovial membrane from a case of 
second type arthritis. The membrane presents an appearance quite different from the one 
peculiar to the first type. Note the fatty and loose-meshed fibrous tissue, and the area of cellular 

infiltration at X. ~ 

and to the new bone. In the knee it is plainly evident, in 
the sjnne or hip it cannot be made out. It is not constant, 
but varies with the progress of the disease. 

The characteristic deformity is slight flexion. Extreme 
deg rees of flexion, such as occur in the first type of arthritis, 
are not met with in this type. In the spine a rounded 










SECOND TYPE OF CHRONIC ARTHRITIS 383 

kyphosis, rarely approaching angularity, is fairly standard. 
Again, the contour ot the spine may be perfectly normal 
with extensive bone changes, or the normal curves may be 
simply slightly changed. Often a lateral curve is the most 
prominent feature. 

The hip, besides being in semiflexion, may be in adduc¬ 
tion or abduction. External rotation is more frequent 
than internal. When the tarsal joints are involved, the 
feet are abducted, flattened and stiff, giving the peculiar 
gait, so beautifully seen in hotel waiters. These are the stiff, 
painful flat feet that have caused so much discussion. 
When the X-rays show the characteristic bone changes, 
the arthritis is thought to be due to the flat feet, whereas 
the flat, rigid feet are the result of the primary arthritis. 
An element of equinus is also present in the deformity, only 
to be distinguished when the foot is brought into adduction. 

Limitation of motion varies according to the joint 
involved, and also with the exacerbations of the disease. 
In spinal disease, with bony ankylosis, the limitation is 
absolute in the region affected. In the spine, in the feet, 
and in the hip, the limitation may be marked. Two ele¬ 
ments enter its causation, namely, muscular spasm, and 
change in the articular surface of the bone. The second 
element is a purely mechanical one. In the spine, flexion 
may be free and extension limited, or the reverse. How- 
ever, the X-rays may show extensive changes in the verte¬ 
brae in the face of a perfectly flexible spine. Rotation, 
adduction, and especially abduction, are all limited in dis¬ 
ease of the hip. A peculiar diagnostic sign in this form of 
arthritis is, that when flexion is forced, the hip goes 
into abduction. 

In the other joints the amount of limitation of motion 
is roughly proportional to the extent of the bone changes. 


384 


INFLAMMATION IN BONES AND JOINTS 


Two physical signs merit attention in this connection. 
In sacro-iliac arthritis, a Kernig sign is present on the 
affected side. It may be present also in lumbar arthritis. 
An Ely sign is often present in lumbar arthritis. 8 

Course of the Disease. —This type of arthritis has 
no set course. It is essentially chronic, and is more or 

less progressive in a joint until 
its cause is removed. Then 
it usually becomes quiescent. 
Its course is influenced by 
trauma, and by hard usage; 
hence partly, the preponder¬ 
ance of patients with laborious 
occupation, though it may be 
said on the other hand that 
people in the poorer classes 
do not take care of their teeth. 
fig. 127.—Articular su.face of head of Tl ie disease occurs in persons 

femur resected eighteen months after frac- x 

ture of the femoral neck in a patient seventy- n ll /-E-. 

three years of age. Note the second ni All 1A11KS, OUL Weil-LO-QO 
type changes. , • . , . . 

patients, who are not driven 
to laborious occupations, usually escape its more pain¬ 



ful manifestations. 

Diet and emotional disturbance also influence the 
course, as do exposure to dampness and cold. Here we 
have the whole clinical picture of the disease. Poor people 
form the majority of the patients, probably because there 
are more poor people than rich. They neglect their teeth, 
but usually have them extracted early, whereas the more 
prosperous person, when his teeth decay, resorts to elab- 


s The patient is laid prone upon the table. If his pelvis rise from the 
table when the surgeon flexes his knee, he is said to have a positive Ely sign. 
The phenomenon is probably caused by the pull forward on the rigid spine 
by the rectus muscle. 




Fig. 128.—Chronic arthritis of the great second type; typical changes in the fingers—Heberden’s nodes. 


SECOND TYPE OF CHRONIC ARTHRITIS 


385 







386 


INFLAMMATION IN BONES AND JOINTS 


orate and expensive dentistry. His mouth is filled with 
dead teeth, crowned, capped and filled. The X-rays show 
the presence of abscesses about the roots of these teeth, 
but they usually occasion no pain, and therefore the patient 
is naturally loath to have the teeth extracted. The poor 
man must work hard, must eat poorly prepared food, and 
is exposed to inclement weather. He is the one therefore 
who suffers most from the severe manifestations of this 
form of arthritis. The prosperous person need do no hard 
physical work, and can keep his body protected from the 
rigors of climate. His food is properly prepared, and he 
can eat what he has learned by experience, will agree with 
him. If his joints become troublesome, he goes to some 
health resort where he is kept quiet, where his diet is care¬ 
fully regulated, and where heat in some form is applied 
to the surface of his body. 

DIAGNOSIS 

This rarely occasions much difficulty. It can be made 
with reasonable accuracy by clinical examination, but it 
can be established beyond peradventure by the X-rays. 
If the bones show the typical lipping and spurring about 
the lines of attachment of the capsule, the arthritis belongs 
in this type. In obscure “neuritides,” “sciaticas” and 
“lumbagos” the spine should be radiographed. 

In a Charcot joint, there may be an irregular produc¬ 
tion of new bone, but it is not in the form of lipping and 
spurring, and it does not follow the line of capsular attach¬ 
ment. Marked disorganization of the joint is present, 
and, instead of limitation of motion, supermobility. The 
Charcot joint is painless, and the patient shows signs 
of tabes. 


SECOND TYPE OF CHRONIC ARTHRITIS 

PROGNOSIS 


387 


The new bone built up 
around the joint is a fixture, 
and shows no tendency to ab¬ 
sorption. Its presence indi¬ 
cates extensive changes in the 
cartilage and in the marrow, 
and its removal therefore is 
not followed by cure. The 
synovial hypertrophy also is 
the indirect result, of the 
changes in the bone and 
cartilage, and there is no ob¬ 
ject in trimming off its villi 
and its redundancies. 

If the cause of the disease 
can be removed before great 
changes have taken place in 
the bone and cartilage, the 
pain may disappear, and the 
joint may return to a state 
approaching normal. With¬ 
out appropriate treatment the 
arthritis has a tendency slowly 
to grow worse. 

This form of arthritis 
carries with it no particular 
danger to life, unless the 
spine be extensively involved. 



Fig. 129. —Chronic arthritis of the great 
second type involving the thoracic spine. 
Note the typical bowing involving a large 
part of the spine. 


In that case respiration may suffer interference, and the 
patient may be liable to pulmonary disease, though rarely 
to tuberculosis. For some unexplained reason, the type 







388 


INFLAMMATION IN BONES AND JOINTS 


of person that is afflicted with this form of arthritis usually 
does not suffer from tuberculosis. 

TREATMENT 

No recognized standard treatment exists for this dis¬ 
ease. The differentiation between the two great types of 



Fig.. 130. The same patient as shown in the preceding figure. In spite of extensive 

disease no real muscular spasm is present. 

chronic arthritis, has never been sharply made by most 
writers, and the treatment recommended for one, usually 
is the same as that recommended for the other. The two 
are entirely different, as has been shown in the preceding 
pages, and should be handled along different lines. 

As I view the disease, the essential pathological feature 
is the aseptic necrosis in the bone near the joint line, and 
the almost invariable cause is the chronic osteomyelitis 
in the alveolar processes of the jaws. I recognize that the 





SECOND TYPE OF CHRONIC ARTHRITIS 


389 


bone and cartilage changes are permanent, and that when 
the architecture of the joint has once been seriously dam- 

w 

aged by this disease, it can never be restored. The prob¬ 
lem of making cartilage grow again over the end of the 
bone is strikingly like that of making hair grow again on 
a bald head. Therefore the best I can do when a patient 
presents himself for treatment, is to stop the disease where 
it is, with the idea that, when I remove the cause, provided 
the bone changes are not excessive, the changes in the soft 
tissues will disappear and the symptoms will subside. 

The first indication is to remove every focus of infection 
from about the roots of the teeth. Its presence usually, 
but not always, can be determined with the X-rays. Dead 
teeth are always to be viewed with suspicion, even when the 
radiogram does not show any rarefaction about their roots. 
They are foreign bodies, and it is doubtful if the bone is 
ever healthy in their immediate vicinity. Sometimes an 
old, buried root is discovered. It must be dug out. The 
wisdom of the so-called “surgical” removal of teeth is at 
present being urged, that is, the necessity of chiselling 
away the alveolar processes. Personally I do not think it 
is necessary. 

The removal of the focus in the mild cases may he all 
the treatment necessary. The symptoms promptly disap¬ 
pear and so does the patient. In the majority of cases 
however some discomfort and stiffness remain. They can 
be made less by physical therapy. Heat in some form is 
almost always grateful to patients with this type of arthri¬ 
tis. Baking, ironing out with a hot flat-iron over several 
layers of blanket, hydrotherapy will all be found useful. 
The so-called Bier treatment, passive hypersemia with the 
employment of the Esmarch bandage, seems to relieve the 


390 INFLAMMATION IN BONES AND JOINTS 

pain in the joints of the extremities. The bandage should 
be applied for an hour or so daily, just tight enough to 
turn the extremity dusky red and warm, not tight enough 
to turn it blue and cold. 

A search for parasites in the stools should be made, 
and if they be found, treatment for their removal should 
be instituted. 

For some reason, the intramuscular injection of a 
foreign protein seems to act favorably in some cases. The 
identity of the proteid is not important. Typhoid vaccine 
will serve, or antigonococcus serum or vaccine. 

We recognize the subsidiary role of cold, dampness, 
strain, emotional disturbance and diet. We keep the 
patients warm, and warn them against exposure, recom¬ 
mending a residence in a suitable climate if possible. 9 
We guard against strain, and regulate the diet according 
to the patient’s idiosyncrasies. Most persons reaching 
adult life know perfectly well what they may safely eat, 
and what they may not, but few have the requisite will 
power to prescribe a diet for themselves. It is a cynical 
way to look at it, but the patient’s idiosyncrasies can be 
extracted from him, and then a suitable diet can be pre¬ 
scribed with the requisite amount of camouflage. In these 
chronic diseases the psychological element must not be 
neglected. All indigestible food is tabu. Generally, 
shell fish, strawberries, tomatoes and red wines are objec¬ 
tionable. Sugar as a rule should be ingested sparingly. 
Red meats do not agree with some people, fish with others. 
Milk, as an article of diet for an adult, is probably greatly 
overrated. Tea, coffee and tobacco, are all poisons that 
agree well with most persons. 


' 9 Climate is not everything in the treatment of this disease. The climate 
of California is renowned, but this type of arthritis is prevalent in California. 




SECOND TYPE OF CHRONIC ARTHRITIS 


391 


My experience teaches me that the treatment outlined 
above is more rational and more satisfactory than any 
other, but the experience of other observers, many of them 
of deservedly high reputation, leads them to entirely differ¬ 
ent conclusions. Like any disease, whose aetiology and 
pathology have not been definitely established, this type of 
arthritis is treated in most diverse ways. 

Pemberton 10 does not differentiate sharply between the 
two great types. He considers chronic arthritis generally 
to be caused by metabolic disturbance, and strongly urges 
its treatment by measured diet. The chief point in his 
thesis, is the harmfulness of the carbohydrates, and he 
reduces their ingestion to a minimum. 

Many observers fail to make the sharp distinction be¬ 
tween the two great types. Many observers make the 
distinction, but think that infection in the tonsil, in the 
jaws or in the deep urethra can cause either type of arthri¬ 
tis indiscriminately, and advise the removal of the focus 
wherever it is found, for either type of arthritis. This 
view, I think, is held by most men whose opinion is of 
value. The exclusive role of alveolar infection is original 
with me, and has not been accepted by anyone except by 

some of mv immediate associates. 

%/ 

All manner of drugs, external applications and physi¬ 
cal therapy, have been recommended. Salicylates often 
will relieve the pain. Strange to say, immobilization is 
not well tolerated by most patients, but in spinal arthritis 
a Taylor brace protects from strain, and sometimes makes 
the pain less. In sacroiliac arthritis a Goldthwait belt 
answers the same purpose. 

10 Pemberton., Ralph : “ The nature of arthritis and rheumatoid conditions.’' 
J. A. M. A ., lxxv, 1759. 

Pemberton, Ralph, and Robertson, J. W.: “ Studies on arthritis in the 
army, etc.” Arch. Int. Med., 1920, xxv, 231. 







INFLAMMATION IN BONES AND JOINTS 


392 

In tarsal arthritis, with accompanying rigid Hat 
foot, Whitman’s treatment is probably the best. Under 
general anaesthesia, Whitman wrenches the foot around 
into strong inversion and dorsal extension, pads it well, 
and puts it up in plaster of Paris for about six weeks. 
At the end of that tune he removes the plaster, takes 
a cast of the foot, and puts the foot up in plaster 
again for a couple of weeks longer. Meanwhile he 
has a Whitman brace fashioned from the cast, and 
has the j^atient's shoe raised a quarter of an inch on the 
inside. When the second plaster dressing is removed, 
active and passive movements are started, and the patient 
wears the brace and the built-up shoe. The result of 
this treatment is usually excellent. 

This type of arthritis in the hip is sometimes very pain¬ 
ful, and the pain may persist in spite of all the ordinary 
methods of treatment. In such case resection offers the 
best way out. The head of the bone should be removed, 
preferably through the Sprengel incision, the trochanter 
should be thrust into the acetabulum, and the hip should 
be immobilized in a long plaster of Paris spica for a month 
or two. Probably the pain which often follows a fracture 
of the femoral neck, in the elderly, is due to this form of 
arthritis. Resection here also will be found satisfactory. 

PRACTICAL CONSIDERATIONS 

In the preceding pages, the investigator should find 
much that will help to a comprehension of the subject of 
chronic arthritis, and to a further advance of knowledge. 
For the general practitioner, who is called on almost daily 
to treat cases of chronic arthritis, a few practical hints may 
be in order. 


SECOND TYPE OF CHRONIC ARTHRITIS 393 

In the first place, one should lay down a hard and 
fast rule, in the absence of distinct motor symptoms, never 
to make a diagnosis of a neuritis or neuralgia of the 
extremities, until a thorough examination, both clinical and 
skiagraphic, has excluded the presence of any lesion of 
the spine. Possibly an isolated peripheral neuritis may 
exist without motor symptoms, hut it is improbable in the 
highest degree. Sciatica, lumbago, brachial neuritis and 
intercostal neuralgia usually can be traced back to a lesion 
of the spinal joints or of the cord itself. 

The patient should be stripped invariably. A woman 
may be draped with a sheet for the examination. Any 
change in the contour of the spine should be noted, and 
then limitation of motion should be sought in any region 
of the column. A lesion of the sacro-iliac joint gives a 
positive Ivernig sign, as a rule. 

An inflammation of any joint of the extremities is 
usually easily detected, if only the patient’s clothes are 
removed, and if the possibility of referred pain is kept in 
mind, especially of pain in the knee with hip joint disease. 
The joint is usually swollen, and almost invariably is lim¬ 
ited in its motion. The latter is the chief diagnostic sign. 

Having determined the presence of an arthritis, the 
next step is to put it in its correct class or type. This 
can usually be done by the clinical examination, and can 
always be done with the aid of the Rontgen rays. The ques¬ 
tion has been dealt with at length in the preceding pages. 

If the arthritis is of the second great type, its cause is 
to be sought in the alveolar processes of the jaws, and any 
infection there is to be removed as the first step in the treat¬ 
ment. The joints must be protected from strain, and 
kept warm, and the diet must be regulated. A search 
should be made for parasites in the stools. 


394 INFLAMMATION IN BONES AND JOINTS 

When the arthritis is of the first great type, the ques¬ 
tion is not always so simple. It can be caused by any one 
of a number of different agents, but the chief ones are the 
tubercle bacillus, the treponema pallidum, and the diplo- 
streptococcus domiciled in the tonsil, or in the deep urethra 
of the male. An absolute clinical differentiation of these 
three is impossible, but the more carefully one searches 
the history and examines the patient, the less frequently 
will one err. 

Tuberculosis may occur at any age, but a persistent 
single arthritis in the young is usually tuberculosis. 
Tuberculosis is slow in its onset and rarely involves more 
than one joint. If the bone is involved, the disease is 
wont to be very painful, and to be accompanied by marked 
muscular spasm and atrophy. Cold abscess practically 
excludes everything else except coccidioidal granuloma. 

Syphilis may be single or multiple in its joint mani¬ 
festations. It may be painless, but often is quite painful. 
The bone may be badly damaged in the immediate neigh¬ 
borhood of the joint, without interference with joint func¬ 
tion. Glandular enlargement is frequent, and other 
evidences of syphilis, especially new periosteal bone forma¬ 
tion. When the gumma breaks down, and when a sinus 
forms, the mouth of the sinus is wont to be dirty, dark red, 
undermined, and sluggish looking, whereas that of tuber¬ 
culosis is pale, puffy, and pouting. 

Diplostreptococcic arthritis, though sometimes single, 
is more often multiple. The joint may be swollen or 
shrunken, full of fluid, or a mass of adhesions. If the 
habitat of the organism is in the deep urethra, the arthritis 
may have supervened on an acute gonococcic infection, or 
it may be chronic from the start. When all is said, we 
usually make the diagnosis on probabilities. Involvement 


SECOND TYPE OF CHRONIC ARTHRITIS 395 

of the finger joints speaks for the tonsil, as does a certain 
tendency to symmetry. Pain under the heels speaks for 
the deep urethra. If examination shows disease of the 
seminal vesicles or prostate, and pus in the tonsillar crypts, 
naturally we should first turn our attention to the urethral 
lesion, for a patient with detritus in the tonsil may be in 
health, but one with a deep urethral lesion never is. On 
the other hand a patient with a lesion in the deep urethra, 
may have an arthritis caused by tonsillar infection, and if 
his arthritis did not recover after treatment of the former, 
then we should remove his tonsils. We do not stop until 
we have done our best to remove every possible focus 
of infection. 

REFERENCES 

Axhausex, G.: “ Ueber einfache, aseptische Knochen- und Knorpelnekrose, 
Chrondritis dissecans und Arthritis deformans.” Arch. f. klin, Chir., 
1912, xcix, 519. 

Axhausen, G.: “Ueber Untersuchungen iiber die Rolle der Knorpelnekrose in 
der Pathogenese der Arthritis deformans.” Arch. f. klin. Chir., 1914, 
civ, 301. 

Axhausen and Pels, Isaac: “ Experimentelle Beitriige zur Genese der Arthritis 
deformans.” Deutsche Ztsclir. f. Chir., 1911, cx, 515. 

Bassoe, Peter: “The late manifestations of compressed-air disease.” Am. 
Jour. Med. Sci., 1913, cxlv, 526. 

Beitzke, H.: “Ueber die sogen. Arthritis deformans atrophica.” Ztsclir. f. 
klin. Med., 1912, lxxiv, 213. 

Billings, Frank : “ Chronic focal infections and their etiologic relations to 
arthritis and nephritis.” Arch. Int. Med., 1912, lx, 484. 

Billings, Frank: “Chronic focal infection as a causative factor in chronic 
arthritis.” Jour. A. M. A., 1913, lxi, 819. 

Billlings, Frank: “Focal infections.” New York and London, 1916, Appleton 
and Company. 

Bruns: “Ueber das Lipoma arborescens des Kniegelenks und seine Bezie- 
hungen zu chronischen Gelenkaffektionen.” Beitr. z. klin. Chir., 1896, 
xvi. 285. 

Bullmore, H. H., and Waterhouse, Rupert: “The blood in rheumatoid 
arthritis.” Edin. Med. Jour., 1907, xxi, 523. 

Burt, J. B.: “The production of Osteophytes and Exostoses in chronic gout 
and arthritis deformans.” Proc. Roy. Soc. Med., 1913-1914, vii, 45. 


390 


INFLAMMATION IN BONES AND JOINTS 


Cecil, Russel L.: “A report on forty cases of acute arthritis treated by the 
intravenous injection of foreign protein.” Arch. Ini. Med., 1917, xx, 951. 
Chapman, H. S.: “The results obtained in the treatment of chronic arthritis 
by the removal of a distant focus of infection.” Ann. Surf/., 1920, lxxi, 648. 
Cowie, David Murray and Calhoun, Henrietta: “Nonspecific therapy in 
arthritis and infections.” Arch. Int. Med., 1919, xxiii, 69. 

Dick, George F.: “Chronic multiple arthritis due to bacillus mucosus.” Jour. 
A. M. A., 1917, lxviii, 622. 

Ely, Leonard W.: “The second great type of chronic arthritis.” Arch. Surg., 
1920, i, 158. 

Ely, Leonard W.: “ The great second type of chronic arthritis; further studies.” 

California State jour. med. 1921, xix, 415. 

Ely,* Leonard W.: “The great second type of chronic arthritis; third study.” 
Calif, state j. med. 1922, xx. 

Erdman, Seward: “The acute effects of caisson disease or aeropatliy.” Am. 
Jour. Med. Sci., 1913, cxlv, 520. 

Erving, William G. : “On the condition of the blood in rheumatoid arthritis 
and osteoarthritis.” Am. Med., 1903, vi, 440. 

Fayerweather, Roades: “Infectious arthritis: a bacteriological contribution 
to the differentiation of the ‘rheumatic’ affections.” Am. Jour. Med. 
Sci, 1905, cxxx, 1051. 

Goldthwait, Joel E.: “ Osteo-arthritis of the spine: spondylitis deformans.” 

Boston Med. Surg. Jour., 1899, cxli, 128. 

Goldthwait, Joel E.: “Osteo-arthritis of the spine; spondylitis deformans. 

(second paper).” Boston Med. Surg. Jour., 1902, cxlvi, 299. 

Goldthwait, Joel E.: “Infectious arthritis.” Boston Med. Surg. Jour., 1904, 
cl, 363. 

Hahn, L.: “ Ueber die Entstehung der Gelenkkorper bei Arthritis deformans.” 

Deutsche Ztsclir. f. Chir., 1919, cxlix, 289. 

Herrick, W. W., and Parkiiurst, G. M.: “Meningococcus arthritis.” Am. 
Jour. Med. Sci., 1919, clviii, 473. 

Hildebrand, O.: “Die Entstehung des Gelenkhydrops und seine Behandlung.” 
Arch. f. klin. Chir., 1906, lxxxi, 412. 

Kimura, K.: “ Histologische Untersuchungen iiber Knochenatrophie und 
deren Folgen, Coxa vara, Ostitis und Arthritis deformans.” Zeigler’s 
Beitr., 1900, xxvii. 225. 

Janssen, Peter: “ Zur Kenntnis der Arthritis chronica ankylopoetica.” Mitt. 

a. d. Grenzgeb. d, Med, u. Chir., 1903, xii, 720. 

Lillie, H. J., and Lyons, H. R.: “Tonsillectomy in myositis and arthritis.” 
Jour. • A. M. A., 1919, lxxii, 1214. 

Lund, Peer M. : “Acute infectious arthritis following pneumonia.” Am. Jour 
Rontgenol., 1919, vi, 457. 

McCrae, Thomas: “ The pathology and etiology of arthritis deformans.” Jour. 
A. M. A., 1904, xliii, 1027. 

McCrae, Thomas: “Arthritis deformans.” Jour. A. M. A.. 1904, xlii, 1, 94 
and 161. 


SECOND TYPE OF CHRONIC ARTHRITIS 397 


Miller, Joseph L, and Lusk, Frank B.: “The treatment of arthritis by the 
intravenous injection of foreign protein.” Jour. A. M. A., 1916, lxvi, 
1756 and Jour. A. M. A., 1916, lxvii, 783. 

Moon, V. H., AND Edwards, S. R.: “Result of blood cultures in rheumatoid 
arthritis.” Jour. Infect. Dis., 1917, xxi, 154. 

Nathan, Philip William: “The differential diagnosis of the diseases hitherto 
grouped together as rheumatoid arthritis, chronic rheumatism, arthritis 
deformans, etc.” Jour. Mecl, Sci., 1906, cxxxii, 857. 

Nathan, P. William: “The etiology, pathology, and classification of certain 
forms of joint disease, with a scheme for the classification of joint 
diseases generally.” Am. Jour. Med. Sci., 1906, cxxxi, 636. 

Nathan, P. W., and Strong, W. W.: “The joint cartilage in its relation to 
joint pathology.” Am. Jour. Orth. Surg., 1909-1910, vii, 85. 

Nathan, Philip W.: “A new and apparently successful method of treating 
metabolic osteo-arthritis.” Jour. A. M. A., 1911, lvi, 1779. 

Nathan, Philip William: “The neurological condition associated with 
polyarthritis and spondylitis. “Am. Jour. Med, Sci., 1916, clii, 667. 

Nichols, Edward II., and Richardson, Frank L.: “Arthritis deformans.” 
Jour. Med. Research, 1909, xxi, 149. 

Pemberton, Ralph: “The nature of arthritis and rheumatoid conditions.” 
Jour. A. M. A., 1920, lxxv, 1759. 

Pemberton, Ralph and Robertson, J. W.: “Studies on arthritis in the 
Army, based on four hundred cases.” Arch. Int. Med., 1920, xxv, 231. 

Pommer, Gustav: “Die funktionelle Theorie der Arthritis deformans vor 
dem Forum des Tierversuehes und der pathologischen Anatomie.” Arch, 
f. O rth op., 1919-1920, xvii, 573. 

Port, K.: “ Einc fur den Orthopaden wichtige Gruppe des chronischen 
Rheumatismus (Knotchenrheumatismus).” Arch f. Orth op., 1919-20, xvii, 
465. 


Rhein, John H. W.: “Pathologic report of the nervous system in a case of 
spondvlose rhizomelique.” Jour. A. M. A., 1908, li, 463. 

Rosenow, E. C.: “The etiology of articular and muscular rheumatism.” Jour. 
A. M. A., 1913, lx, 1223. 

Rosenow, E. C.: “Transmutations within the streptococcus pneumococcus 
group.” Jour. Infect. Dis., 1914, xiv, 1. 

Rosenow, E. C.: “Etiology of arthritis deformans.” Jour. A. M. A., 1914, 
lxii, 1146. 

Ruffer, Armand: “Arthritis deformans and spondylitis in ancient Egypt.” 
Jour. Path, and Bacter., 1918, xxii, 152. 

Schmidt, Rudolph: “ Zur klinik der Gelenkerkrankungen.” Med. Klin., 1912, 
viii, 1485. 

Schuller, Max: “ Untersuchungen iiber die Aetiologie der sogen. chronisch- 
rheumatischen Gelenkentzundungen.” Bert. klin. Wochnsch., 1893, xxx, 865. 

Schuller: “ Chronisch-rheumatische Gelenkentziindung.” Berl. klin. Wch- 
nschr., 1896, xxxiii, 172. 


398 INFLAMMATION IN BONES AND JOINTS 

Schulman, M.: “Parenteral protein treatment of arthritis, with special refer¬ 
ence to milk injections, its relation to anaphylaxis."’ Med. Rec., 1920, 
xcviii, 47. 

S ievers, Roderick : “ Die Arthritis acromio-clavicularis als wichtiges Glied in 
der Pathologie der stumpfen Schulterverletzungen.” Deutsche Ztschr. 
f. Chir., 1914, cxxix, 583. 

Snyder, R. G.: “A clinical report of nonspecific protein therapy in the treat¬ 
ment of arthritis.” Arch. Int. Med., 1918, xxii, 224. 

Strangeways, T. P. S.: “Morbid anatomy and histology of rheumatoid arth¬ 
ritis.” Brit. Med. Jour., 1918, ii, 623. 

Walkhoff: “Ueber Arthritis deformans.” V erhandl. d. Deutsch. Path . 
Gesellsch., 1905-1906, ix-x, 229. 

Weichselbium, A : “Die senilen Veranderungen der Gelenke und deren 
Zusammenhang mit der Arthritis deformans.” Wien. k. Akad. der 
Wissensch. Math. Natur. Wissensch. Classe., 1877, lxxv, 193. 

White, W. Hale: “On the pathology of acute rheumatoid arthritis.” Guy’s 
Hosp. Reports, 1902, lvii. 9. 

Wollenberg, Gustav Albert: “ Die Aetiologie der Arthritis deformans im 
Lichte des Experimentes.” Arch. f. Orthop. etc., 1909, vii, 226. 


SECTION VIII 


ARTHRITIS CAUSED BY DEVELOPMENTAL 

ABNORMALITIES 



























CHAPTER I 


LEGG’S DISEASE 

There are three diseases or conditions of the joints of 
the lower extremity, one in the hip, one in the knee, and 
one in the foot, whose exact nature never has been estab¬ 
lished, but which present marked similarity in more than 
one respect. Each one comes at a certain age, each affects 
boys more than girls, and all three are generally considered 
to be caused by trauma, though the infectious origin of 
one is at present being urged. Each causes an arthritis. 
The three are Legg’s disease, the “essential ’ joint mouse, 
and Koehler’s disease. 

Legg’s disease affects the epiphysis of the femoral head, 
and gives symptoms between the ages of five and ten, when 
the bone nucleus is at a certain state of development. The 
typical joint mouse forms in the medial condyle of the 
femur of adolescents, and gives symptoms just before the 
union of the lower femoral epiphysis with the shaft; 
Koehler’s disease always affects the navicular bone of the 
foot, gives symptoms between the ages of three and nine, 
and causes no trouble when ossification of the navicular is 
finished. For these reasons, although the evidence is by 
no means conclusive, the grouping of the three lesions 
is justified. 

On the hypothesis stated, the developmental abnormal¬ 
ity may exist indefinitely without causing any symptoms. 
The joint however, considered as a machine, is defective, 
and is easily damaged. A slight injury, which, in a nor¬ 
mal joint would occasion no trouble, here starts up an 
arthritis. In other words the arthritis occurring with these 
deformities, is to be considered as a traumatic arthritis. 

401 


26 


402 INFLAMMATION IN BONES AND JOINTS 

LEGG’S DISEASE 

Perthes’ Disease; Osteochondritis Deformans 
Juvenilis; Arthritis Deformans Juvenilis 

This disease was described almost simultaneously by 
Legg of Boston, by Calve of France and by Perthes of 
Leipzig, Legg antedating Calve by about five months. 
Perthes followed Calve in three months. It consists 
of a peculiar segmentation and change in shape of the 
femoral head. 

^Etiology. —Nothing definite is known as to this. 

The disease is generally considered to be caused by an 

infection. In two cases, a growth of staphylococcus is 

said to have been recovered from a soft area in the neck of 

the femur. Boys are more often affected than girls in about 

the proportion of 4-1. The typical changes of the disease 

are often observed in the Bontgen picture of congenital 

dislocations of the hip which have been reduced. They have 

been discovered accidentally also on several occasions in 

•/ 

the sound hip of patients who have been operated upon for 
congenital dislocation. Like most joint diseases, this has 
been ascribed to trauma and to syphilis. LTntil the publica¬ 
tion of Legg’s paper, it was mistaken for tuberculosis, and 
probably the vogue of certain methods of treating hip 
tuberculosis in the past, has been due to this error. 1 

The things which speak for the view that Legg’s dis¬ 
ease is essentially caused by a congenital anomaly of 
development of the proximal bone nucleus of the femur, 
are the following: 

1. The condition is observed almost invariably at a 
certain period of growth. Practically all the patients are 
between the ages of five and ten. 

1 The writer has been guilty of this error. In his book on joint tubercu¬ 
losis appears a Rontgen picture of a case of cured hip tuberculosis. In the 
light of increased knowledge this is evidently a case of Legg’s disease. 



LEGG’S DISEASE 


403 


2. The typical deformity may exist indefinitely with¬ 
out symptoms, and may be discovered accidentally. 

3. The condition is frequently bilateral. 

4. It is seen often with congenital dislocation of the 
hip, not only in the affected hip after reduction, but also 
on the sound side. 

5. An infection in the epiphysis severe enough to 
produce the bone changes which actually occur, would 
sometimes undoubtedly break into the joint and cause 
an infectious arthritis. No case of actual suppuration is 
on record. 

6. When the case is properly treated, the bone slowly 
forms in the epiphysis, and a cure regularly results in about 
a year, with little deformity or with none at all. Without 
treatment, the deformity slowly increases, and terminates 
in a characteristic condition. The details of the argument 
can be supplied from a study of the symptomatology and 
of the scant pathological findings. If we faced an infec¬ 
tion, the pathological material at our disposal would be 
far richer than it is. 

Pathology. —As to this we know very little. Two 
operators claim to have recovered at operation a pure 
culture of staphylococcus from the marrow of the neck 
of the femur. One of these cases showed a “necrotic” 
area, the other a “grayish” condition of the marrow. 
Perthes excised a piece of synovial membrane and a piece 
of the femur head from one patient. The synovial mem¬ 
brane was normal. The bone showed irregular islands 
of cartilage in the marrow, near the articular cartilage. 
Neither the marrow nor the synovial membrane showed 
any sign of inflammation. 

Phemister operated upon one case. The joint was full 
of a slightly turbid, straw-colored fluid, and the* synovial 
membrane was villous. An excised tag of the membrane 


404 


INFLAMMATION IN BONES AND JOINTS 


showed “hyperplastic connective tissue elements with a 
few areas of round cell infiltration and a thickened synovial 
covering rich in nuclei.” He found a cavity in the epiphy- 



Fig. 131. Legg’s Disease. Note the irregularity in the epiphysis. 

sis filled with granulation tissue and necrotic debris. The 
striking feature in his specimen is the dead bone. Many 
larger and smaller sequestra could be seen in the material 
scraped out of the cavity in the epiphysis. Under the 
microscope, the dead trabecula; could be made out. 



405 


LEGG’S DISEASE 

Symptomatology. —The thing for which a patient 
with Legg s disease almost invariably is brought for treat¬ 
ment is the limp. As a rule the limp is painless, though 
occasionally the child may complain of slight discomfort 
when he becomes tired. 

On examination the extremity is seen to be in an indif¬ 
ferent attitude, or in one of slight adduction. Moderate 
muscular atrophy may be present but no real muscular 
spasm. The characteristic limitation of motion in this 
disease is in abduction. This is almost always decidedly 
compromised. Sometimes all abduction is abolished. 
Rotation as a rule is also restricted. Other motions may 
or may not be limited. In testing the range of motion 
a peculiar phenomenon usually can be brought out. When 
flexion is forced, the thigh goes into slight abduction, as 
it does in the second great type of arthritis. 

Measurement shows the lower extremities to be of the 
same length, or possibly a shortening of about a centimetre 
in the affected extremity. The trochanter is prominent. 
In untreated cases the prominence of the trochanter 
increases, as does the shortening, and the limitation of 
abduction if this last has not been extreme from the start. 
The typical result of an untreated case is coxa vara, that is, 
a shortened, bent neck of the femur. 

The disease runs its course in two or three years, with 
an active period of about one year. The constitution does 
not become affected, and the j^atient often runs and plays 
with his fellows. 

The diagnosis may be made tentatively on the sympto¬ 
matology, but it is clinched by the skiagram. This is 
characteristic. 

The Rontgen rays show: 


406 INFLAMMATION IN BONES AND JOINTS 

1. A flattening, broadening, and sometimes a lat¬ 
eral displacement, of the femoral epiphysis, with one 
or more divisions of it, and irregularity of ossification. 



Fig. 132. —Legg’s Disease. Note the irregularity in the epiphysis. 


2. An irregularity or even a segmentation of the 
epiphysial disc. 

3. Loss of bony structure of the neck, especially of its 
proximal and lateral part. 




LEGG’S DISEASE 


407 


4. Irregularity of contour of the proximal border of 
the femoral neck. 

5. Distortion of the head. 

The first two are perhaps the most constant and im- 



Fig. 133.—Legg’s Disease. Note the irregularity in the epiphysis. 

portant of these signs. In addition may be mentioned 
the occasional enlargement of the great trochanter. Occa¬ 
sionally also an irregularity in the outline of the acetabu¬ 
lum can be distinguished. What strikes the observer in 





408 INFLAMMATION IN BONES AND JOINTS 

all this, is the marked disproportion between the extensive 
bone changes and the insignificant clinical symptoms. 

Whatever its cause, evidently a softening of the 
femoral neck, especially that part of the neck in the region 
of the epiphysial line, is present. If the neck is exposed 
to weight bearing in the normal attitude, the epiphysis 
is displaced laterally more and more, and becomes more 
and more distorted, the neck bends and becomes thicker 
and shorter. 1 his is the condition shown in the skiagram 
of the late stages of untreated cases, and it is probable that 
many cases of coxa vara in the adolescent are simply the 
end stages of an unrecognized previous Legg’s disease. 

TREATMENT 

Opinions differ as to this. I * hen lister operated upon 
his patient, cleaning out the necrotic area in the epiphysis, 
and got a good result. Practically all other authorities 
advise conservative treatment. Perthes believes in mas¬ 
sage and physical therapy, others recommend the traction 
brace to relieve the femoral neck from weight bearing. 
An excellent form of treatment is to abduct the hip to its 
extreme range, and put it up in that position in a short 
plaster spica. This forced abduction should be kept up 
with renewed spicas for a year or two, or until the Rontgen 
rays show a solidification of the femoral neck, and a more 
or less complete ossification of the epiphysis. 


CHAPTER II 

LOOSE BODIES IN THE JOINT 

Joint Mouse 

"Osteochondritis Dissecans” 

When we speak of a joint mouse we have a rather 
clear conception of our meaning in our mind, but when we 
attempt to give the term an exact definition, we find that 
the task is somewhat difficult. A joint mouse is a piece 
of bone or cartilage, or of bone and cartilage, loose in the 
joint, or attached to the capsule by a pedicle. However, 
not all pieces of loose cartilage are included in this cate¬ 
gory. As the result of tuberculosis in the marrow, larger 
or smaller fragments of cartilage are thrown off into the 
joint cavity, but these are not considered joint mice. 
Again in tabetic arthropathy, masses of bone and cartilage 
are separated, and lie in the joint, but these also are not 
joint mice. A joint fracture might occasion the presence 
of a piece of bone in the joint, but in the early stages of 
the trouble we should not call this a joint mouse. If, 
however, the fracture healed, the symptoms subsided, and 
the joint returned to an approximately normal condition, 
and if thereafter, the loose bone fragment should occasion 
trouble mechanically by its presence, we would speak of it 
as a joint mouse. 

Islands of bone or cartilage are sometimes formed in 
the synovial membrane in the second great type of arthritis 
(: i.e “arthritis deformans,” hypertrophic arthritis, degen¬ 
erative arthritis, osteoarthritis, etc.), but they are not 
regarded as joint mice unless they constitute the main 
source of complaint, and overshadow the causal trouble, 

409 


410 


INFLAMMATION IN BONES AND JOINTS 


then, whether they are loose or are still attached by a 
pedicle they are spoken of as joint mice. Otherwise they 
are simply recognized as bone and cartilage formations 
at operation. It is this factor of clinical importance that 
modifies our definition, and viewed in this light joint mice 
are of three kinds: first those which result from fracture, 



Fig. 134.—Joint mice in the elbow. 

second those which result from arthritis of the second great 
type, and third, the real “essential’’ joint mouse, formed 
in the articular end of a bone, usually the medial condyle 
of the femur. 

As to the origin of the first class, there seems to be 
little discussion. If we believe that a fracture can cause the 
separation of a piece of bone and cartilage from the normal 
joint end of a bone, it is easy to understand that it will 
thereafter be loose in the joint cavity and constitute a 


411 


LOOSE BODIES IN THE JOINT 

joint mouse. Such an occurrence, however, must be very 
rare, and while admitting the possibility, I confess that 
I have never seen a clear case of this kind. 

The second class is more numerous. The islands of 
cartilage in the synovial membrane, occurring in the great 
second type of arthritis, may remain attached to the mem¬ 
brane, or may be loosened. It is likely that bone may be 
developed in them. Again it is possible that cartilage 
and bone may be broken off from the circumference of the 
articular ends of the hone, that is, 
from the new bone and cartilage 
that result from the lipping and 
exostoses in this form of arthritis. 

I have in my possession a stained 
slide from a piece of cartilage, 
about 5 m. in diameter, removed 
at hip resection. It was from one 

n i „ , . . n tl Fig. 135. — Two joint mice removed, 

ot these cases ot arthritis ol the exact size, from the elbow shown 

in Fig. 135. The lines on one show 

hip, shows well-marked calcifica- where the section from h was taken - 

tion, has a capsule of fibrous tissue and presumably was 
formed in the synovial membrane. 

The third kind of joint mouse has occasioned much 
discussion. To account for its origin, two theories have 
been put forward. Koenig and his disciples maintain that 
a trauma to the end of the femur causes a localized necrosis 
in the bone end, and that a subsequent reactive inflamma¬ 
tion separates this necrotic bone and cartilage, and sets 
it free. To this process Koenig gives the name “osteo¬ 
chondritis dissecans.’' Axhausen has attempted to prove 
this theory by wounding the articular cartilages of labora¬ 
tory animals with an electric needle. 1 His views have 
•/ 

1 Axhausen: “ Ueber einfache aseptische Knochen und Knorpelnekrose, 
Chondritis dissecans und Arthritis deformans.” Archiv. fur Klinische Chir- 
urgie, 1912, xcix, 519. 







412 


INFLAMMATION IN BONES AND JOINTS 


obtained wide acceptance. Three sets of experiments 
carried out by Cowan and Ely, 2 throw grave doubt on the 
correctness of Axhausen’s conclusions. In this connection 
it may be remarked that there can be no mechanical inj ury 
to a bone without a fracture. 

Barth and his followers attribute these joint mice 



• ' • .i 

Fig. 136. Photograph of a section of the larger of the mice shown in 
the preceding figure. X about 4 diameters. 

directly to trauma, and deny the existence of any dissect¬ 
ing inflammation. They maintain, in other words, the 
fracture theory. 

Several objections can be urged against these two 
theories. 

In the first place, tuberculosis furnishes the best pos¬ 
sible example of an osteochondritis dissecans, yet it never 

3 Ely and Cowan: “Bone and Joint Studies 1.” Stanford University, 
Cal. Published by the University, 1916. 






413 


LOOSE BODIES IN THE JOINT 


produces a typical joint mouse. It gives rise to an inflam¬ 
mation in the marrow which kills the bone trabeculae, and 
often throws a sequestrum of bone and pieces of cartilage 
into the joint. Examined under the microscope, these 
have no resemblance to a joint mouse. 

By Koenig’s explanation, a trauma injures the bone 
end, hut exactly what could the injury be, that would 
cause this resulting dissecting inflammation? The soft 
tissues in the bone are beauti¬ 
fully protected from all injuries 
except fracture. 

Against the fracture theory 
may be urged the fact that the 
injury which starts the trouble 
is not, as a rule, a severe one, and, 
as was said above, cases of de¬ 



monstrated fracture with a dis- „ T 

r ig. lo7.—Low power photograph of 

tinct history, rarely are followed the smal aboSt/dfaiieieL mice * x 

by these joint mice. Again, various writers have published 
cases of typical joint mouse in which the articular cartilage 
was intact over them, and the joint mouse lay held in its 
bed by the intact cartilage. A subcartilaginous fracture 
would be almost unthinkable. 

There are three peculiar things about the joint mouse: 
1st, its structure; 2nd, its location; 3rd, the age of the 
patient. It usually is found in young male adults or 
adolescents. 

When one studies a joint mouse under the microscope, 
one is struck by the resemblance of its structure to that 
observed in foetal bones during the stage of intracartila- 
ginous ossification. The resemblance is marked. 

The location in the medial condvle has been mentioned. 


414 


INFLAMMATION IN BONES AND JOINTS 


The age at which these joint mice begin to give trouble,, 
is that at which ossification in the lower epiphysis draws 
near completion, and the epiphysis joins to the shaft— 
about 20 years. 

The “essential” joint mouse is always single, but the 
other variety may be multiple. 

It seems then that neither of the best known theories 
of the origin of the true joint mouse is correct, and that 
the condition is due to an anomaly in the development of 
the distal epiphysis of the femur, possibly to an extra 

centre of ossification which fails 
to unite with the rest of the 
epiphysis. 

Symptomatology.— L o o s e 
bodies are far more frequently 
met with in the knee than in any 
other joint, and their sympto¬ 
matology is markedly similar to 
that of a torn semilunar cartilage. 
Indeed, by the very definition of a loose body, the torn 
semilunar might be included, but for the sake of clearness 



Fig. 138.—Loose body removed from 
joint, natural size. 


it is well to keep the two things separate in our minds. 
One is essentially from the bony structure, the other from 
the soft parts. 

In the great majority of cases the history starts with 
a trauma, and, as a rule, the trauma is not great. The 
patient, in jumping, or falling, injures his knee. The 
joint swells, and exhibits all the signs of an acute traumatic 
arthritis. The arthritis subsides, and the joint usually 
returns to normal, and remains so until the body becomes 
pinched between the joint ends. The joint may lock, and 
the patient fall to the ground. Again, a simple sprain 
may result, a rupture of part of a ligament. The synovial 




415 


LOOSE BODIES IN THE JOINT 

membrane is torn, and blood pours into the joint. A 
number of these attacks may weaken the joint, and give 
iise to a more or less chronic arthritis. 

Diagnosis. Oftentimes these loose bodies can be felt 
through the skin. The patient may be able to locate them 



Fig. 139.—Rontgenogram showing defect in surface of condyle of femur 
produced by the separation of the piece of cartilage. 


himself. The greater number, those that consist partly of 
bone, can be detected with the Rontgen rays. 

Treatment. —This consists exclusively of operative 
removal. After the body has been located, an incision is 
made through a convenient part of the joint capsule, and 
the body is caught with a pair of forceps and is removed. 
If there are others they should be removed also. Scrupu- 





416 


INFLAMMATION IN BONES AND JOINTS 



Fig. 140.—Typical joint mouse from medial condyle of the knee; photograph of stained 
slide of section from the joint mouse shown in Fig. 138. The marked square represents the 

area taken for the next illustration. 



Fig. 141.—Low power photomicrograph of the marked portion of the preceding. The 
picture here presented strongly suggests intracartilaginous ossification. 





417 


LOOSE BODIES IN THE JOINT 

lous care should be exercised in asepsis. The finger 
gloved or ungloved, should not be inserted into the joint.’ 
It is often inserted, and of course the procedure gives one 
the sense of thoroughness, but it is unecessary and dan¬ 
gerous. Suture of the capsule, and of the superficial 
tissues, completes the operation. 

Sometimes the joint mouse will be found lying in its 
bed in the medial condyle of the femur, from which it never 
has departed. One must not forget at operation, those 
laie cases in which the intact articular cartilage holds the 
otherwise loose body in place. These cases show no sign 
at operation, of the joint mouse in spite of the fact that 
the X-rays have shown its presence. One tests out the 
cartilage by pressure, incising it where it yields. 


27 


CHAPTER III 


KOEHLER’S DISEASE 

Definition. —A peculiar disease, or more properly, a 
peculiar condition, consisting in an abnormal shape, size 
and density of the tarsal navicular bone, first described by 
Koehler, of Wiesbaden, in 1908. 

^Etiology. —Boys are more often affected than girls 
in about the proportion of two to one. The age limits 
appear to be one and ten years. The great majority of 
cases are met with between the ages of three and seven, 
and five is the age at which the condition most often is seen. 

Infection and trauma have been held responsible for 
Koehler’s disease, but nothing that we know of the effects 
of trauma and infection upon bone indicates that either 
of them could cause the condition revealed by the Rontgen 
rays. The peculiar shape and consistency of a certain 
hone observed at a certain stage of development, which 
always disappears as growth proceeds, constitutes a strong 
argument that Koehler’s disease is due to a developmental 
anomaly. Its occasional bilateral occurrence increases 
the strength of the argument. 

Symptomatology. —Either following an injury, or 
spontaneously, pain is felt over the navicular bone. This 
pain is made worse by exercise. Sensitiveness is also 
present, and with it may be associated swelling and redness. 
The patient limps, and may walk on the lateral border of 
the foot to save the medial part of it. 

The symptoms persist for a longer or shorter time, 
and then disappear. They may last for a few weeks, or 

418 



419 


KOEHLER’S DISEASE 

for a few months. Complete recovery always takes place 
under any treatment. 

r ^ I he diagnosis is made by means of the Rontgen rays. 
These show the peculiar shape and consistency of the navi¬ 
cular bone. It is narrow, that is, the distance from its 
proximal border to its distal is diminished, but the gap 
between the talus and the cuneiform, indicates the presence 
of cartilage on each side of the bone nucleus. The bone 
itself is irregular in outline, and very dense in structure, 
so dense that the bone architecture, as ordinarily seen in 
the plate, is absent. The shadow is much darker than 
that of the neighboring bones. 

Treatment. H his is largely a matter of indifference. 
If the foot is protected from injury and strain, the patient 
will probably be more comfortable. 


CHAPTER IV 


OSGOOD-SCHLATTER DISEASE 

Osgood’s Disease, Schlatter’s Disease 

Somewhat akin to the preceding group, is a painful 
condition of the tubercle of the tibia, described first by 
Osgood , 1 and a few months later by Schlatter . 2 Its under¬ 
lying cause is a peculiar formation of the proximal epiphy¬ 
sis of the tibia, but the symptoms probably owe their 
origin to trauma. Authorities differ as to the exact nature 
of the complaint, and it is necessary, in the first place, to 
exclude from the category cases of distinct fracture of 
the tibial tuberosity, though this injury produces a clinical 
picture hardly to be distinguished from that of Osgood- 
Schlatter disease. 

If a large number of X-ray plates of the proximal 
end of the adolescent tibia he examined, the majority 
will show the epiphysis to have the shape of a fairly regu¬ 
lar disc. A large proportion will show anteriorly a distal 
prolongation of the epiphysis in the form of a beak, or horn. 
This peculiar bone development is not to be regarded as 
at all abnormal in itself. It occurs too frequently for that, 
and its existence causes no symptoms. It is to be viewed 
simply as an irregularity, but as an irregularity which 
predisposes to injury. Sometimes the beak is quite regu¬ 
lar, sometimes it is roughened or segmented, but its pres¬ 
ence seems to predispose to this so-called disease. 

1 Osgood, Robert B.: “ Lesions of the tibial tubercle occurring during 
adolescence.” Boston Med. and Surg. J., 1903, v. 148, 114. 

2 Schlatter, Carl: “ Verletzungen der schnabelfoermigen Fortsatzes der 
oberen Tibiaepiphyse.” Beit. zur. klin. Cliir., 1903, v, 38, 874. 


420 



OSGOOD-SCHLATTER DISEASE 421 

Most authorities agree that trauma stands in a causal 
relation to the symptoms, though some hold to the infec¬ 
tious theory, and some predicate a congenital tendency to 
general aberrant epiphysial development. Whether the 
trauma is direct upon the epiphysial beak, or indirect by 



Fig. 142.—Osgood-Schlatter Disease. 

pull of the quadriceps tendon, is still a matter of debate. 
Probably it can be either. In this connection, Heron’s 
observation, that, when the beak is present, it serves for 
the attachment of the patellar tendon, is important. 
Strong contraction of the quadriceps muscle then would 
tend to loosen the epiphysis. This would result in a con¬ 
dition analogous to a chronic sprain. The situation of the 
beak, on the other hand, exposes it to direct violence. 

Osgood-Schlatter disease is seen only in the young. 
Symptoms may present themselves apparently at any time, 
from the appearance of the ossific centre in the proximal 




422 


INFLAMMATION IN BONES AND JOINTS 


epiphysis, until union of the epiphysis with the shaft. 
Seven to eighteen years may be said to be about the limits. 



Fig. 143.—Osgood-Sclilatter Disease. 

Authorities differ markedly as to the most vulnerable age. 
Some find the condition oftener in the right leg, some in the 
left. As with Legg’s disease, joint mouse, and Koehler’s 
disease, boys are afflicted much more frequently than girls. 


OSGOOD-SCHLATTER DISEASE 


423 


Often the peculiar 
beak is present on both 
tiba?, on one without 
symptoms. Rontgen 
pictures taken for other 
conditions about the 
knee sometimes dis¬ 
close the beak as an 
accidental finding. Oc¬ 
casionally the conti¬ 
nuity of the beak with 

%/ 

the epiphysis is broken, 
and a separate centre 
for the tubercle re¬ 
places the beak. 

Symptomatology. 

—The patient, usually 
a young boy, complains 
of more or less pain in 
the exact location of the 
tibial tubercle, and 
often gives a history of 
an injury of not severe 
degree. Examination 
shows moderate swell- 

ing, Without fluctua- FIG. 144. —Osgood-Schlatter Disease. 

tion, or crepitation. The swelling, is extremely sensitive 
to pressure, and may be reddened, but never ecchymotic. 

The diagnosis is made with the Rontgen rays. They 
show the peculiar bone development at the tibial tuberosity, 
usually in the form of a beak, and more or less notched 
and irregular. 










424 INFLAMMATION IN BONES AND JOINTS 

Various operations have been recommended for this 
affection, but the3 r seem unnecessary. Massage or strap¬ 
ping with adhesive tape suffices for the milder cases. The 
more severe ones yield to immobilization with plaster 
of Paris. 

ARTHRITIS FROM CONGENITAL ANOMALY 

OF THE PATELLA 

Attention has been called by several writers to irregu¬ 
larities in the development of the patella as well as to the 
presence of a bipartite or supernumerary j)atella, and these 
irregularities have been assumed, with reason, to be the 
cause of attacks of synovitis in young adults, recurring 
after strenuous physical exertion. They are revealed by 
the Rontgen rays. 

The treatment is that of any mild traumatic arthritis. 
No one has proposed as yet, any treatment of the causal 
anomaly. It seems to incapacitate a patient for hard 
physical exercise, such as marching. 

GOUTY ARTHRITIS 

The characteristic lesions of this form of arthritis are 
the necroses in the bone and cartilage, and the deposition 
of crystals of biurate of sodium in the bone, in the cartilage, 
and in the capsule. The arthritis itself, is probably the 
result of these gross primary changes, and is therefore 
essentially a traumatic arthritis. 

The diagnosis is made on the chalky deposits in the 
region of the joints, especially in the region of the meta¬ 
tarsophalangeal joint of the great toe. The X-ray picture, 
with its punched out areas in the bone near the articular 
surface, is quite characteristic. In the fingers the dis¬ 
ease, must be carefully distinguished from the second great 
type of arthritis, the so-called Heberden’s nodes. 


OSGOOD-SCHLATTER DISEASE 


425 


Possibly gout may be caused by some form of 
protozoon. 

BIBLIOGRAPHY 


LEGG’S DISEASE 

Allison, Nathaniel and Moody, Ellsworth: “Osteochondritis deformans 
juvenalis (Perthes’ disease).” Am. Jour. Orth. Surg., 1915, xiii, 197. 
Brandes, Max: “ Ueber Spatdeformationen bei reponierter kongenitaler Hiift- 
gelenksluxation und ihre Verhiiltnis zum Krankheitsbilde der Osteochon¬ 
dritis deform, juvenil.” Ztschr. f. Orthop. Chir., 1915, xxxv, 274. 

Brunn, Max: “Ueber die juvenile Osteoarthritis deformans des Hiiftgelenks.” 
Beitr. z. klin. Chir., 1903, xl, 650. 

Calve, Jacques: “ Sur une forme particuliare de pseudo caxalgie.” Rev. 
Chir., 1910, xlii, 54. 

Delitala: “Contribution for the study of a typical disease of the upper 
end of the femur. (Perthes’ disease).” Am. Jour. Orth. Surg., 1914-1915, 
xii, 555. 

Ely, Leonard W.: “ Legg’s disease.” Ann. Surg., 1919, lxix, 47. 
Frangenheim, Paul: “ Zur Pathologie der Osteoarthritis deformans juvenilis 
des Hiiftgelenks, ueber Coxa vara und traumatische Epiphysnlosung am 
oberen Femurende.” Beitr. z. klin. Chir., 1909, lxv, 19. 

Kidner, F. C.: “Perthes’ disease.” Am. Jour. Orth. Surg., 1916, xiv. 339. 
Legg, Arthur T.: “ An obscure affection of the hip-joint.” Boston Med. Surg., 
Jour., 1910, clxii, 202. 

Nieber, Otto: “Ueber Osteochondritis deformans coxae juvenilis.” Ztschr. f. 
Orthop. Chir., 1915, xxxv, 301. 

Perthes, Georg: “Ueber Arthritis deformans juvenilis.” Deutsche Ztschr. 
f. Chir., 1910, cvii, 111. 

Perthes, Georg: “Ueber Osteochondritis deformans juvenilis.” Arch. f. 
klin. Chir., 1913, ci, 779. 

Phemister, D. B.: “Operation for epiphysitis of the head of the femur. 

(Perthes’ disease).” Arch. Surg., 1921, ii, 221. 

Schwartz, Erwin: “ Eine typische Erkrankung der oberen Femurepiphyse.” 
Beitr. z. klin. Chir., 1914, xciii, 1. 


JOINT MOUSE 


Boerner, E.: “Klinische und pathologisch-anatomische Beitriige zur Lehre 
von den Gelenkmausen.” Deutsche Zeitschr. f. Chir., 1903-1904, lxx, 363. 
Brehm O. : “Zur Kasuistik der Gelenkmiiuse.” Deutsche Ztschr. f. Chi)., 

1913, cxxiv, 81. 


Budinger, Konrad: “Ueber Ablosung von Gelenkteilen und verwandte 
Prozesse.” Deutsche Ztschr. f. Chir., 1906, lxxxiv, 311. 

Freiberg A H. and Wooley, Paul G.: “Osteochondritis dissecans: con¬ 
cerning its nature and relation to formation of joint mice.” Am. Jour. 
Orth. Surg., 1910-1911, viii, 477. 


426 


INFLAMMATION IN BONES AND JOINTS 


Heineck, Aime Paul: “Joint bodies from within and from without present 
in articulations otherwise apparently normal.” III. Med. Jour., 1915. 
xxviii, 1. 

Kappis, Max: “ Ueber Bau, Wachstum and Ursprung der Gelenkmaiise.” 
Deutsche Ztschr. f. Chir., 1920, clvii, 214. 

Kappis, Max: “ Zur Lehre von den Gelenkmausen.” Deutsche med. Wchnschr., 
1920, xlvi, 1161. 

Kappis, Max: “Osteochondritis dissecans und traumatische Gelenkmause.” 
Deutsche Ztschr. f. Chir.., 1920, clviii, 187. 

Lfhmann: “Zur Frage der Entstehung der freien Gelenkkorper vom rbntgen- 
ologischen Standpunkt.” Fortschr. a. d. Geb. d. Rontgenstrahlen., 1911- 
1912, xviii, 397. 

Lindenstein: “Osteochondritis dissecans und Gelenkmause.” Beitr. z. klin. 
Chir., 1906, li, 503. 

Mosenthal, A.: “Grosses Corpus liberum im Talocruralgelenk.” Berl. klin . 
Wchnschr.. 1912, xlix, 1892. 

KOEHLER’S DISEASE 

Fassett, F. J.: “Isolated disease of the scaphoid.” J. Am. Med. Ass., Chicago; 
1914, lxii, 1155. 

Hetzel, W. B.: “Isolated disease of the scaphoid bone of the foot (Koehler’s 
disease).” Am. J. Orthop. Surg., Bost., 1917, xv, 214217. 

Koehler, A.: “Ueber eine haufige, bisher anscheinen unbekannte Erkrankung 
einzelner kindlicher Knochen.” Miinchen. med. Wchnschr., 1908, lv, 1923. 

Pfahler, G. E.: “Isolated disease of the scaphoid bone of the foot in 
children (Koehler's disease).” Surg., Gynec. and Obst., Chicago 1913, 
xvii, 625-627. 

McClure, Chas. R.: “Isolated disease of the scaphoid.” J. Am. M. Ass., 
Chicago; 1918; lxxi, 1360-1361. 

Sonntag, E.: “ Beitrage zur koehlerschen Krankheit des Kahnbeins am Fusse 
bei Kindern.” Deutsche Ztschr. f. Chir., clxiii, 145. 

Stumme: “ Kompressions fracture des Knochenkerns des Os naviculare pedis.’* 
Fortschritte a. d. Gebiete d. Rontgenstrahle, 1911, xvi, 342. 

OSGOOD-SCHLATTER DISEASE 

Altschul, Walter: “Zur Aetiologie der schlatter’schen Erkrankung.” Beitr. 
z. klin. Chir., 1919, cxv, 741. 

Bergman, W.: “Ueber die Entwickelung der Tuberositas tibiae und ihre 
typische Erkrankung in der Adolescenz.” Arch. f. klin. Chir., 1909. lxxxix, 
477. 

Dunlop, John: “The adolescent tibial tubercle.” Am. Jour. Orth. Surg., 
1912, ix, 313. 

Graef, Wilhelm: “Ueber Schlatter’sche Krankheit.” Beitr. z. klin. Chir., 
1914-15, xcv, 647. 

Kawamura, K.: “ Beitrag zur Osgood-Schlatterschen Krankheit.” Acta 

Scholce Medicinalis, 1917-18 ii, 99, 


OSGOOD-SCHLATTER DISEASE 


427 


Mcllf.r, Walther: “Multiple spontane Epiphysenlockerungen und Frak- 
turen in der Adoleszenz.” Beitr. z. klin. Chir., 1920, cxx, 389. 

Osgood, Robert B.: “Lesions of the tibial tubercle occurring in adolescence.” 

Boston Med. Surg. Jour., 1903, cxlviii, 114, 127. 

Schlatter, C.: “ Unvollstiindige Abrissfrakturen der Tuberositas tibiae oder 
Wachstumsanomalien?” Beitr. z. klin. Chir., 1908, lix, 518. 

Schlatter, Carl: “ Verletzungen des schnabelformigen Fortsatzes der oberen 
Tibiaepiphyse. Beitr. z. klin. Chir., 1903, xxxviii, 874. 

Solieri, S.: “Sulla cura operatoria della malattia di Osgood-Schlatter.” 
Chir., degli, organi di mov., 1921, v, 353. 

CONGENITAL ANOMALIES OF THE PATELLA 

Hodgson, F. G.: “The tubercle of the tibia. . .” Am. Jour. Orth. Surg., 1918, 
xvi, 116. 

Kempson, F. C.: “ Emargination of the patella.” Jour. Anat. Physiol., 1902, 
xxxvi, 419. 

Salmond, R. W. A.: “The recognition and significance of fractures of the 
patellar border.” Brit. Jour. Surg., 1918-19, vi, 463. 

Todd, T. W.: “Defects of the patellar border.” Ann. Surg., 1921, lxxiv, 775. 
Wright, Wm. : “A case of accessory patellae in the human subject. . .” 
Jour. Anat. Physiol., 1903-04, xxxviii, 65. 






INDEX OF AUTHORS 


A K 


Addis, Thomas, 123 

Albee, Fred, 54 

Albee and Morrison, 47 

Aleison and Brooks, 68 
Axhausen, G., 411 

Kirsciiner, M., 70 

Klemm, P., 81 

Kocher, T., 70 

L 

B 

Lagrange, 184 

Baer, W. S., 68, 70, 107 
Bamberger, E., 156 

Bartit, A., 53 

Brickner, W. M., 83 

Lexer, E., 22, 81, 182 

M 

MacEwen, W., 36 

C 

Marie, P., 156 

Mauclaire, P., 64, 184 

Corner, E. M., 69 

von Mikulicz, J., 229 
Mosciicowitz, E., 35 

Murphy, John B., 67, 71, 96 

E 


Ely and Cowan, 367, 412 

N 

F 

Neuber, G., 91 

Nichols, E. H., 41, 89, 159, 181 
Nichols and Richardson, 371 

Findlay, L., 158 

Finotti, E., 316 

Fraenkel, E., 20, 100 

O 

Ollier, E., 36, 64, 67, 184 

G 

Ophuls, W. M., 348 

Geddes, A. C., 34 

P 

H 

Paget, J., 148 

Parrot, M. J., 136 

Hahn, O., 312 

Hamilton, P. G., 91 

Helferich, 67 

Payr, E., 68 

Pemberton, R., 391 

Perrin, 110 


429 


430 


INDEX OF AUTHORS 


R 

Roevsing, Tl)., 180 
R ollier, A., 219 
Rosenow, E. C., 349 

S 

Schede, M., 91 
Senn, N., 91 
Sever, J. W., 309 
Smitii-Petersen, M. N., 70 
Sprengel, 70, 179 
Stile, G. T., 360 
Sumita, M., 68 


T 

Taylor, R. W., 137 

V 

Van Hook, W., 331 

W 

Waldeyer and Koebner, 136 
Wegner, G., 136 
Whitman, R., 181 


INDEX 


A 

Albee hip operation, 288 
Albee spine operation, 260 
Amoeba in chronic arthritis, 369, 390 
Ankylosis, 60 

Ankylosis, treatment of, 66 
Arthritis, acromio-clavicular, 318 
acute, suppurative, haematogenous, 
94 

chronic, 173 

chronic, classification of, 174 
chronic, practical considerations in, 
392 

chronic, progressive, multiple, 357 
chronic, developmental anomalies 
causing, 399 

chronic, developmental anomaly of 
patella causing, 423 
contagious disease causing, 97 
deformans, 365 
deformans juvenilis, 402 
degenerative, 365 
diplostreptococcic, 349 
gonococcic, 103 
gouty, 355, 424 
hypertrophic, 365 
pneumococcic, 97 
proliferative, 349 
rheumatoid, 349 
second great type, 365 
suppurative, from wounds, 120 
syphilitic, 141 
traumatic, 112 
tuberculous, 177 
typhoid, 100 
Arthroplasty, 67 

B 

Beck’s paste, 92, 230 
Bilroth’s hinges, 301 
Bipp, 93 


Bone, composition of, 15 
Bone, formation of, 32 
Bone, transplantation of, 49 
Bow legs in rickets, 163 
Braces in joint tuberculosis, 224 
Bradford frame, 258 
Brodie’s abscess, 83 
Bursitis, subacromial, 318 

C 

Calot formula, 220 
Calot head sling, 264 
Calot jacket, 264 
Callus, external, 42 
Callus, internal, 41 
Carcinoma, 215 
Caries sicca, 200, 317 
Carrel-Dakin treatment, 122 
Cottrell treatment for sprain of ankle. 
Cartilage, semilunar, fracture of, 114 
Cartilage, structure of, 24 
Cold abscess, treatment of, 220 
117 

Coxa Vara, 278 
Craniotabes, 162 

D 

Dactylitis, syphilitic, 139 
Dactylitis, tuberculous, 339 

E 

Ely operation on the wrist, 329 
Ely sign, 118, 384 
Endosteum, 16 

Epiphysis, separation of in syphilis, 
138 

F 

Fenwick operation on the knee, 306 
Fibrolysin, 67 
Fracture, healing of, 41 
Fracture, non-union of, 45 


431 


432 


INDEX 


G 

Giant cell growth, 156, 215 
Gout, 355, 424 
Guinea pig test, 212 

H 

Haemarthrosis, 123 
Haemophiliac joints, 123 
Halisteresis, 41 
Harrison’s groove, 162 
Heberden’s nodes, 378 
Heliotherapy, 219 
Hibbs knee operation, 305 
Hibbs sacro-iliac operation, 333 
Hibbs spine operation, 254 
Hydrarthrosis intermittens, 110 
Hyperaemia, passive, 229 

I 

Incision. Kocher’s, for hip resection, 
291 

Murphy’s on the hip, 292 
Murphy’s, for temporomaxillary 
ankylosis, 71 
Smith-Petersen’s, 290 
Sprengel’s on the hip, 70, 290 
on knee joint, 305 
Injection treatment in joint tuber 
culosis, 229 

J 

Joint, definition of, 24 
Joint fungus, 200 
Joint mouse, 409 

K 

Knee, Fenwick operation on, 306 
Hibbs operation on, 305 
tuberculosis of, 295 
Knock knee in rickets, 163 
Koehler’s disease, 417 
Kyphosis, 237, 244 

L 

Legg’s disease, 278, 402 
Leontiasis ossea, 155 
Ligament, 24 

Loose bodies in the joint, 409 


M 

Marrow, injury of, 79 
structure of, 18 
Metaphysis, 82 
Morbus coxae senilis, 377 
Mosetig-Moorhoff’s paste, 92 
Myeloma, benign, 156 

O 

Oidium coccidioides, 346 
Osgood’s disease, 419 
Osgood-Schlatter’s disease, 419 
Osteoarthritis, 365 

Osteoarthropathy, pulmonary hyper¬ 
trophic, 156 
Osteoblast, 32 

Osteochondritis deformans juvenilis, 
402 

Osteochondritis dissecans, 409 
Osteochondritis syphilitica, 137 
Osteoclast, 34 
Osteomalacia, fatty, 191 
Osteomyelitis, acute suppurative 
haematogenous, 79 
albuminosa, 81- 
chronic, 131 
fibrosa, 155 

following compound fractures, 99 
gonococcic. 103 

mother of pearl workers’, 134 
Osteotomy, hip joint disease, after, 286 
Osgood’s, on the knee, 304 
Ostitis deformans, 148 
fibrosa, 147 
productive, 21 
rarefying, 21 

P 

Paget’s deforming, 148 
sclerosing, 134 
serosa, 84- 
typhoid, 100 
Perichondrium, 25 
Periosteum, 22 

role of in healing of fractures, 46 
Periostitis, syphilitic, 142 


INDEX 


433 


Perthes’ disease, 402 
Phosphorus necrosis, 133 
Plaster of Paris dressings, 226 
Plaster of Paris jacket, 263 
Plaster of Paris spica, 281 
Pott’s disease, 237 
Pott’s paraplegia, 248 
treatment of, 267 
Pseudarthrosis, treatment of, 49 
Pseudoparalysis, 138 
Psoas abscess, 246 
treatment of, 268 

R 

Rachitis, Rhachitis, 158 
Rheumatism, acute inflammatory, 108 
Rice bodies, 201 
Rickets, 158 
Rosary, rachitic, 162 

S 

Saber shin, 141 

Sacro-iliac joint, Hibb's approach to, 
333 

Smith-Petersen’s approach to, 335 
Sarcoma, 215 
Schlatter’s disease, 419 
Scoliosis, 251 
Scorbutus, 163, 214 
Scurvy, 163, 214 

Smith-Petersen operation on sacro¬ 
iliac joint, 335 
Spine, Albee operation on, 260 
Spine, Hibb’s operation on, 254 
tuberculosis of, 237 
Spina ventosa, 339 
Sprain, 113 
Sprain of elbow, 117 
Sprain of knee, 114 
Sprain of spine, 118 
Sprain of wrist, 117 
Sprengel’s incision, 290 
Stiffness following fracture, 113 


Still’s disease, 360 

Synovial membrane, structure of, 27 
Synovitis, intermittent, 110 
syphilitic, 145 
Syphilis, bone, of, 135 
congenital, early, 136 
differentiation of, 212 
osseous in adult, 141 

T 

Tabetic joints, 146 
Taylor spinal brace, 259 
Thomas hip splint, 283 
Thomas knee splint, 302 
Torticollis, 251 
Traction hip splint, 284 
Tumor albus, 201, 297 
Tuberculin test, 211 
Tuberculosis, ankle, 308 
calcaneus, 312 
cold abscess in, 202, 209 
differentiation of from syphilis, 212 
elbow, 322 

fingers and toes, 337 
fracture in, 193 
hip, 272 
joints, 177 
knee, 295 
ribs, 341 

sacro-iliac joint, 331 
shoulder, 317 
spine, 237 

sternoclavicular joint, 341 
tarsus, 312 
wrist, 326 

Typhoid arthritis, 100 
Typhoid spine, 101 

W 

White swelling, 201, 297 
Whitman-Bradford frame, 258 
Whitman treatment for flat foot, 392 
Wrist, Ely operation on, 329 
































































































































































